Basic Emotions

[Petter]

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3624960/

Role of right pregenual anterior cingulate cortex in self-conscious emotional reactivity

Self-conscious emotions such as embarrassment, shame, guilt and pride are social emotions in which the self stands at the forefront of awareness. Our use of the term ‘self’ in this context refers to one’s physical being, as well as the thoughts and feelings that constitute the subjective sense of that being (James, 1890). These emotions serve important interpersonal functions (Miller and Leary, 1992; Tangney, 1999; Lewis, 2000). Embarrassment, for example, typically arises when heightened attention is paid to the self after violation of a social rule (Keltner, 1995). Not only is embarrassment associated with autonomic nervous system responding including increases in heart rate, blood pressure, sweating (Keltner, 1995; Harris, 2001; Gerlach et al., 2003) and peripheral vasodilation (producing characteristic facial blushing), but it also has a characteristic behavioral display (e.g. smile control, gaze aversion and face touching; Shearn et al., 1990; Keltner, 1995). The physiological and behavioral changes that occur in embarrassment signal to others that one regrets the offending action (Miller, 2007) and may help motivate actions (e.g. apologizing) that redress social transgressions.

[OFC] may be important for the regulation, and not generation, of self-conscious emotion (Beer et al., 2003)

ACC 1.png

[Petter]

https://www.jneurosci.org/content/41/47/9742.abstract

The subgenual (sgACC) and perigenual cingulate (pgACC) have distinct structural and functional characteristics and are important afferent modulators of the amygdala. The sgACC is critical for arousal, whereas the pgACC mediates conflict-monitoring, including in social contexts.

[Petter]

https://neuro.psychiatryonline.org/d...np.23.2.jnp121

Simple emotions activate ACC, with pACC more responsive to happiness and sACC to sadness. Induction of sadness increases subjective ratings of pain and pain-related activation of the MCC. Reward also activates the ACC; sACC activity correlates with the expected value of options. Action-selection and expression of learned fear are more likely to activate pMCC, whereas tasks requiring cognitive control, conflict-monitoring, error-detection, or emotion- (including fear) related appraisal (evaluation) are more likely to activate aMCC and perhaps pACC. Activations related to emotional conflict-regulation and fear-inhibition during extinction are more likely in the sACC. Reappraisal activates both aMCC and sACC. Thus, MCC is “cognitive”— involved in conflict-monitoring and response-selection and execution. Within MCC, aMCC is implicated in emotional appraisal, conflict-monitoring, approach–avoidance decisions, and willed control of actions. pMCC is involved in body-orientation and movement-execution. ACC is “affective,”— involved in emotion assessment, emotion-related learning, and autonomic regulation. Within ACC, pACC is implicated in emotional regulation, autonomic integration, and affect related to pain. sACC is implicated in autonomic control, visceral integration, and conditioned learning.

[Petter]

https://emotiontypology.com/positive...on/excitement/

You experience excitement as high arousal, accompanied by the feeling of ‘butterflies in your stomach’, trembling, or sweaty palms. Your increased heart rate, breathing and perspiration prepare you for physical action. These jittery bodily feelings are somewhat atypical for a positive emotion, and more akin to negative emotions like fear or nervousness, with the difference that you experience them as positive.

[Petter]

https://www.ncbi.nlm.nih.gov/books/NBK537192/

interest: attention, learning, goal-directed behavior (---> a potential reward or threat)

https://en.wikipedia.org/wiki/Emotion#Components

Bodily symptoms: the physiological component of emotional experience.

This does not apply to interest so it is not a basic emotion.

[Petter]

A)

1. the need for pleasure and avoidance of pain <--> euphoria and dysphoria (---> +/- mood)

2. the need for control/orientation (achieve goals) <--> basic emotions

3. the need for attachment (cooperation: safety needs, work, play, care) <--> laughing and crying (<--- 1 and 2)

4. the need for self-esteem enhancement (social hierarchy: show off achievements) <--> pride and shame

B)

1. the need for pleasure and avoidance of pain <--> excitement, (sham) rage, fear

2. the need for control/orientation (achieve goals) <--> frustration, euphoria and dysphoria (---> +/- mood)

3. the need for attachment (cooperation: safety needs, work, play, care) <--> laughing and crying (<--- 1 and 2)

4. the need for self-esteem enhancement (social hierarchy: show off achievements) <--> pride and shame

[Petter]

hypothalamus

1: LH, DMH, VMH, AHN, PVN (cortisol and thyroid), PH (SNS)

2 and 4: the mammillary bodies, PH

3: mPOA, SON (oxytocin)

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excitement: LH

(sham) rage: DMH, VMHvl

fear: VMHdm/c → PAG and VMHdm/c → AHN pathways mediate immobility and avoidance, respectively

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https://i.imgur.com/4Jpnjte.jpg

[Petter]

(see post #445)


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9164627/

The ventral tegmental area (VTA) is well known for regulating reward consumption, learning, memory, and addiction behaviors through mediating dopamine (DA) release in downstream regions. Other than DA neurons, the VTA is known to be heterogeneous and contains other types of neurons, including glutamate neurons. In contrast to the well-studied and established functions of DA neurons, the role of VTA glutamate neurons is understudied, presumably due to their relatively small quantity and a lack of effective means to study them. Yet, emerging studies have begun to reveal the importance of glutamate release from VTA neurons in regulating diverse behavioral repertoire through a complex intra-VTA and long-range neuronal network. In this review, we summarize the features of VTA glutamate neurons from three perspectives, namely, cellular properties, neural connections, and behavioral functions. Delineation of VTA glutamatergic pathways and their interactions with VTA DA neurons in regulating behaviors may reveal previously unappreciated functions of the VTA in other physiological processes.




https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4339667/

The ventral tegmental area (VTA) in the brain’s reward circuitry is composed of a heterogeneous population of dopamine, GABA, and glutamate neurons that play important roles in mediating mood-related functions including depression. These neurons project to different brain regions, including the nucleus accumbens (NAc), the medial prefrontal cortex (mPFC), and the amygdala. The functional understanding of these projection pathways has been improved since the extensive use of advanced techniques such as viral-mediated gene transfer, cell-type specific neurophysiology and circuit-probing optogenetics. In this article, we will discuss the recent progress in understanding these VTA projection-specific functions, focusing on mood-related disorders.




https://www.vumc.org/cowan-lab/human-euphoria

Drug abuse and addiction pose major health problems to individuals worldwide. The brain biology of drug addiction is thought to involve a variety of brain structures that evolved to have a role in natural rewards, such as finding food or having sex. Drugs of abuse are used in part because they make an individual "high" or euphoric when they are taken.

Much of the evidence learned thus far about drug addiction suggests that regions of the brain, including the ventral tegmental area which uses the neurotransmitter dopamine, and the nucleus accumbens have a major role in reward and the experience of euphoria. Additional evidence indicates that humans reliably develop a high voltage electroencephalographic (EEG) waveform in the alpha band during the experience of euphoria. We propose to use the functional magnetic resonance imaging (fMRI) blood oxygen level dependent (BOLD) method to study the regional changes in brain activity during the experience of euphoria in humans.

[Petter]

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3873746/

Dopaminergic neurons in the ventral tegmental area (VTA) are thought to encode reward prediction error - the difference between an expected reward and actual reward.




https://en.wikipedia.org/wiki/Habenula#Lateral_habenula

Then, Bromberg-Martin et al. (2011) highlighted that neurons in the lateral habenula signal positive and negative information-prediction errors in addition to positive and negative reward-prediction errors.




https://pubmed.ncbi.nlm.nih.gov/35616407/

VTA is known to receive projections from LHb and project to the prefrontal cortex and hippocampus.

[Petter]

https://psycnet.apa.org/doiLanding?d...037%2Fh0054548

The purpose of this study was to test the applicability of the frustration-aggression hypothesis to the social behavior of albino rats. The same animals were used as in two previous studies (see 20: 518, 519). After 21 hours of food deprivation, the rats in the experimental series were matched for bouts under three conditions, an empty cage, a single pellet in the cage, and a food hole permitting one rat at a time. In the control series, the rats found food in their cages all the time except during bouts. All three experimental conditions showed fewer aggressions than the control series, and the third condition was significantly below the control in dominance-subordination. The animal in possession of the pellet tended to be more aggressive than its partner, and success at the food hole appeared to be independent of fighting. In explaining these results, the author suggests that frustration is not the only cause of aggression, that the presence of a strange animal is another cause, and that "mental capacity limits the conditions under which organisms can respond to frustration with aggression."




https://onlinelibrary.wiley.com/doi/full/10.1002/ab.22092

In this article, we offer a reconceptualization of the frustration–aggression hypothesis (Dollard et al., 1939), arguably one of the most classic and influential hypotheses in the history of psychology. Whereas its initial, bold version portrayed frustration as both a necessary and a sufficient condition for aggression, subsequent versions toned down this claim and portrayed frustration as necessary but insufficient (Miller, 1941; Sears, 1941). Our analysis suggests that frustration prompts aggression to the extent that it is subjectively demeaning and connotes to the person a loss of their significance (hence, of personal worth and dignity). In turn, the aggressive reaction is a primordial way of demonstrating power and dominance, which are valued attributes that bestow significance on the actor. Although it is primordial, aggression-born dominance is only one way to attain significance. Alternative ways include culturally sanctioned values (e.g., generosity, courage, honesty, creativity, beauty, competence), which confer significance on the actor. When those alternative values are salient and accessible to the individual, the individual may embrace them instead of engaging in aggression. Moreover, when the value of dominance/power is salient and accessible, the individual may engage in aggression without a prior humiliating frustration. Finally, when limited cognitive resources prevent the individual from considering alternative values, aggression may be the ubiquitous reaction to humiliation. In short, then, we recast the frustration–aggression theory as a special case of significance quest, which is dependent on the conditions of its activation (through significance loss, or opportunity for gain), the individual's cognitive resources, and the saliency/accessibility of alternative means to significance that are culturally accepted.

[Petter]

https://i.imgur.com/ACSWUdc.jpg

https://nba.uth.tmc.edu/neuroscience...chapter05.html

The anterior thalamic nuclei in turn connect to the cingulate cortex. The cingulate cortex projects back to the entorhinal cortex of parahippocampal gyrus, completing a “great” loop called the Papez circuit. The Papez circuit like many other areas of the limbic system is involved in learning and memory, emotion, and social behavior, and was originally thought (by James Papez) to the anatomical substrate of emotional experience. The amygdala, along with neocortical areas, are now known to be centrally involved in emotional experience. Its connections to the original Papez circuit are shown in the next figure and the amygdala and emotion are discussed more thoroughly in the next section.

The hippocampus has direct connections to the entorhinal cortex (via the subiculum) and the amygdala. These structures connect to many other areas of the brain. The entorhinal cortex projects to the cingulate cortex. Therefore, the hippocampus can affect the cingulate cortex through the anterior thalamic nucleus or the entorhinal cortex. The cingulate cortex, in turn, projects to the temporal lobe cortex, orbital cortex, and olfactory bulb. Thus, all of these areas can be influenced by the hippocampus.




https://en.wikipedia.org/wiki/Brodmann_area_11

Brodmann area 11 is one of Brodmann's cytologically defined regions of the brain. It is in the orbitofrontal cortex which is above the eye sockets (orbitae). It is involved in decision making, processing rewards, and encoding new information into long-term memory.




https://i.imgur.com/PffVU0s.jpg

https://en.wikipedia.org/wiki/Dorsal_tegmental_nucleus

As part of the Papez circuit, the DTN receives input from habenula neurons and lateral mammillary neurons.




https://en.wikipedia.org/wiki/Latero...mental_nucleus

The laterodorsal tegmental nucleus (LDT) sends cholinergic (acetylcholine) projections to many subcortical and cortical structures, including the thalamus, hypothalamus, substantia nigra (dopamine neurons), ventral tegmental area (dopamine neurons), cortex (with bidirectional connections with the prefrontal cortex).

The laterodorsal tegmental nucleus may be involved in modulating sustained attention or in mediating alerting responses, and also in the generation of REM sleep (along with the pedunculopontine nucleus).

[Petter]

https://www.sciencedirect.com/topics...itual-behavior

Habitual behaviors are often advantageous, as they decrease the cognitive demand necessary to produce behaviors, whereas goal-directed behaviors require constant feedback about the relationship between the behavior and the outcome (Coutureau and Killcross, 2003; Dickinson, 1985), which is advantageous when contingencies change within the environment.

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goal-directed behavior

1. input: learning

2. output: problem-solving or decision-making (facts and/or imagination + logical reasoning and/or a comparison between two objects or choices)

[Petter]

https://en.wikipedia.org/wiki/Habit#Goals

The habit–goal interface or interaction is constrained by the particular manner in which habits are learned and represented in memory. Specifically, the associative learning underlying habits is characterized by the slow, incremental accrual of information over time in procedural memory. Habits can either benefit or hurt the goals a person sets for themselves.

Goals guide habits by providing the initial outcome-oriented motivation for response repetition. In this sense, habits are often a trace of past goal pursuit. Although, when a habit forces one action, but a conscious goal pushes for another action, an oppositional context occurs. When the habit prevails over the conscious goal, a capture error has taken place.

Behavior prediction is also derived from goals. Behavior prediction acknowledges the likelihood that a habit will form, but in order to form that habit, a goal must have been initially present. The influence of goals on habits is what makes a habit different from other automatic processes in the mind.




https://en.wikipedia.org/wiki/Muscle_memory

The basal ganglia also play an important role in memory and learning, in particular in reference to stimulus-response associations and the formation of habits. The basal ganglia-cerebellar connections are thought to increase with time when learning a motor task.

[Petter]

https://en.wikipedia.org/wiki/Caudate_nucleus

Meanwhile, behavioral studies provide another layer to the argument: recent studies suggest that the caudate is fundamental to goal-directed action, that is, "the selection of behavior based on the changing values of goals and a knowledge of which actions lead to what outcomes."

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https://i.imgur.com/YhADeY9.png

[Petter]

https://www.ncbi.nlm.nih.gov/books/NBK557407/

The caudate nucleus (CN; plural “caudate nuclei”) is a paired, “C”-shaped subcortical structure which lies deep inside the brain near the thalamus. It plays a critical role in various higher neurological functions. Each caudate nucleus is composed of a large anterior head, a body, and a thin tail that wraps anteriorly such that the caudate nucleus head and tail can be visible in the same coronal cut. When combined with the putamen, the pair is referred to as the striatum and is often considered jointly in function. The striatum is the major input source for the basal ganglia, which also includes the globus pallidus, subthalamic nucleus, and substantia nigra. These deep brain structures together largely control voluntary skeletal movement. The caudate nucleus functions not only in planning the execution of movement, but also in learning, memory, reward, motivation, emotion, and romantic interaction. Input to the caudate nucleus travels from the cortex, mostly the ipsilateral frontal lobe. Efferent projections from the caudate nucleus travel to the hippocampus, globus pallidus, and thalamus.

[...]

The anterior portion of the caudate nucleus is connected with the lateral and medial prefrontal cortices and is involved in working memory and executive functioning. One can think of the head of the caudate nucleus as the cognitive and emotional portion. The head of the caudate nucleus and medial frontal pole are connected strongly, while the middle section of the caudate nucleus receives input from throughout the prefrontal cortex. The tail of the caudate nucleus interacts with the inferior temporal lobe to help process visual information and control movement. Some caudate nucleus neurons show selectivity for specific visual properties such as direction and spatio-temporal relationships.

[...]

Association learning is another important function of the caudate nucleus. It plays a role in connecting visual stimuli with motor responses as well as learning with feedback. Lesions of the anterior caudate nucleus result in abnormal behavior, which does not correspond to rewards. Specifically, the body and tail of the caudate nucleus are principally involved in learning acquisition while the head of the caudate nucleus has involvement in processing feedback on learning trials. The volume of the right caudate nucleus and the strength of its connections with the hippocampus showed a correlation in one study with performance in memory competitions. The right posterodorsal body of the caudate nucleus exhibits activation, which is specific to seeing a photo of a romantic partner. The medial dorsal striatum is involved in goal-directed and flexible behavior. There is evidence that the mediodorsal striatum is involved in working memory and may be vital to the formation of certain kinds of memories. The anterior caudate nucleus encodes both spatial information and reward and risk information simultaneously and redundantly with the frontal cortex, with which it has strong connections.

Lesions to the caudate nucleus and resulting deficits can further elucidate caudate nucleus function. Lesions to the caudate nucleus can result in abulia, or absence of will, an interesting outcome when considered in conjunction with evidence of its role in goal-directed behavior and motivation. Cats with bilateral caudate nucleus damage were hyperactive and compulsively followed any moving sensory target. These findings reflect the deficits seen in human individuals with obsessive-compulsive disorder, ADHD, autism, and Tourette syndrome, in which the caudate nucleus is implicated (discussed below).





https://news.mit.edu/2018/neuroscien...on-making-0809

In the new study, the researchers wanted to see if they could reproduce an effect that is often seen in people with depression, anxiety, or obsessive-compulsive disorder. These patients tend to engage in ritualistic behaviors designed to combat negative thoughts, and to place more weight on the potential negative outcome of a given situation. This kind of negative thinking, the researchers suspected, could influence approach-avoidance decision-making.

To test this hypothesis, the researchers stimulated the caudate nucleus, a brain region linked to emotional decision-making, with a small electrical current as animals were offered a reward (juice) paired with an unpleasant stimulus (a puff of air to the face). In each trial, the ratio of reward to aversive stimuli was different, and the animals could choose whether to accept or not.

This kind of decision-making requires cost-benefit analysis. If the reward is high enough to balance out the puff of air, the animals will choose to accept it, but when that ratio is too low, they reject it. When the researchers stimulated the caudate nucleus, the cost-benefit calculation became skewed, and the animals began to avoid combinations that they previously would have accepted. This continued even after the stimulation ended, and could also be seen the following day, after which point it gradually disappeared.

This result suggests that the animals began to devalue the reward that they previously wanted, and focused more on the cost of the aversive stimulus. “This state we’ve mimicked has an overestimation of cost relative to benefit,” Graybiel says.





https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3288226/

Early models of the basal ganglia assigned to the caudate a primary role of integrating information from the cortical association and sensorimotor areas of the brain before sending it to distinct ventrolateral thalamic sub-regions, which would then relay the information almost exclusively to the primary motor cortex. These early models have largely been replaced by more complex ones based on evidence of reciprocating but interconnected circuits that link the cortex, basal ganglia, and thalamus (DeLong, Georgopoulos et al. 1983; Alexander, DeLong et al. 1986; Alexander and Crutcher 1990). Five primary circuits have been proposed in the nonhuman primate literature: motor, oculomotor, dorsolateral prefrontal, lateral orbitofrontal, and anterior cingulate (Alexander, DeLong et al. 1986).





https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3079445/

Functional imaging studies have reported with remarkable consistency hyperactivity in the orbitofrontal cortex (OFC), anterior cingulate cortex (ACC), and caudate nucleus of patients with Obsessive-Compulsive Disorder (OCD).

[Petter]

https://www.frontiersin.org/journals...019.00028/full

Figure 1. Characteristics of the shift from goal-directed to habitual behavior. (A) Left: Goal-directed and habitual behaviors are competitive processes that act in balance. Goal-directed behavior is characterized by a high requirement for attention, is highly contingent on present reward value, and demonstrates flexibility of responding. Habitual behavior is stimulus-driven, less dependent on present reward value, and governed by behavioral automaticity. Right: Addiction/compulsion represents an extreme state of habit. (B) The transition from goal-directed behavior to habitual behavior and then into compulsion, or addiction is graded. Shift from goal-directed to habitual behavior and then to compulsion/addiction corresponds to strengthened stimulus-response association and reduced action-outcome contingency. These processes are bidirectional, i.e., a behavior can shift on the spectrum from goal-directed to habitual performance, and back again—though in the extremes of addiction whether it is possible to return fully to habit/goal-directed states is less clear. (C) During instrumental training, rates of responding for a reward increase. Post-training reward devaluation reduces response rates more quickly for goal-directed behaviors than it does for habitual behaviors, which take many more extinction trials to fully dissipate. The extremes of addiction are characterized by compulsive responding that is resistant even to punishment. (D) The balance between goal-directed and habitual behavioral states corresponds to relative levels of neural activity in the dorsomedial (DMS) vs. dorsolateral (DLS) striatum. (E) Task-bracketing activity pattern emerges in the DLS as animals are over-trained on a rewarded behavioral sequence (e.g., running a T-maze for a tasty reward). Spiny Projection Neurons (SPNs) exhibit high activity at the beginning of a learned motor sequence and again at the end as the animal approaches the reward. Fast-spiking interneurons (FSIs) exhibit high activity during the middle stages of a behavioral sequence.

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https://i.imgur.com/0gdCCNz.jpg

[Petter]

https://www.nature.com/articles/nrn1747

Hedonic experience is arguably at the heart of what makes us human. In recent neuroimaging studies of the cortical networks that mediate hedonic experience in the human brain, the orbitofrontal cortex has emerged as the strongest candidate for linking food and other types of reward to hedonic experience. The orbitofrontal cortex is among the least understood regions of the human brain, but has been proposed to be involved in sensory integration, in representing the affective value of reinforcers, and in decision making and expectation. Here, the functional neuroanatomy of the human orbitofrontal cortex is described and a new integrated model of its functions proposed, including a possible role in the mediation of hedonic experience.





https://www.researchgate.net/figure/...fig1_232499483

4 Hedonic hotspots and hedonic circuits of the brain. Opioid hedonic hotspots are shown in nucleus accumbens, ventral pallidum, and brainstem parabrachial nucleus. Neurochemical signals in each hedonic hotspot can cause ampli cation of core 'liking' reactions to sweetness. Hedonic circuits connect hotspots (red) into integrated loops for causation of 'liking' (orange and red loops). Additional forebrain loops relay 'liking' signals to limbic regions of prefrontal cortex and back to hotspots, perhaps for translation of core 'liking' into conscious feelings of pleasure and cognitive representations (dotted, orange cortex). Dashed, black subcortical lines show mesolimbic dopamine projections, which we suggest fail to cause 'liking' after all.





https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4733335/

Converging evidence identifies trait optimism and the orbitofrontal cortex (OFC) as personality and brain factors influencing anxiety, but the nature of their relationships remains unclear. Here, the mechanisms underlying the protective role of trait optimism and of increased OFC volume against symptoms of anxiety were investigated in 61 healthy subjects, who completed measures of trait optimism and anxiety, and underwent structural scanning using magnetic resonance imaging. First, the OFC gray matter volume (GMV) was associated with increased optimism, which in turn was associated with reduced anxiety. Second, trait optimism mediated the relation between the left OFC volume and anxiety, thus demonstrating that increased GMV in this brain region protects against symptoms of anxiety through increased optimism. These results provide novel evidence about the brain–personality mechanisms protecting against anxiety symptoms in healthy functioning, and identify potential targets for preventive and therapeutic interventions aimed at reducing susceptibility and increasing resilience against emotional disturbances.





https://en.wikipedia.org/wiki/Orbitofrontal_cortex

Multiple functions have been ascribed to the OFC including mediating context specific responding, encoding contingencies in a flexible manner, encoding value, encoding inferred value, inhibiting responses, learning changes in contingency, emotional appraisal, altering behavior through somatic markers, driving social behavior, and representing state spaces. While most of these theories explain certain aspects of electrophysiological observations and lesion related changes in behavior, they often fail to explain, or are contradicted by other findings. One proposal that explains the variety of OFC functions is that the OFC encodes state spaces, or the discrete configuration of internal and external characteristics associated with a situation and its contingencies. For example, the proposal that the OFC encodes economic value may be a reflection of the OFC encoding task state value. The representation of task states could also explain the proposal that the OFC acts as a flexible map of contingencies, as a switch in task state would enable the encoding of new contingencies in one state, with the preservation of old contingencies in a separate state, enabling switching contingencies when the old task state becomes relevant again. The representation of task states is supported by electrophysiological evidence demonstrating that the OFC responds to a diverse array of task features, and is capable of rapidly remapping during contingency shifts. The representation of task states may influence behavior through multiple potential mechanisms. For example, the OFC is necessary for ventral tegmental area (VTA) neurons to produce a dopaminergic reward prediction error, and the OFC may encode expectations for computation of RPEs in the VTA.

Specific functions have been ascribed to subregions of the OFC. The lateral OFC has been proposed to reflect potential choice value, enabling fictive(counterfactual) prediction errors to potentially mediate switching choices during reversal, extinction and devaluation. Optogenetic activation of the lOFC enhances goal directed over habitual behavior, possibly reflecting increased sensitivity to potential choices and therefore increased switching. The mOFC, on the other hand, has been proposed to reflect relative subjective value. In rodents, a similar function has been ascribed to the mOFC, encoding action value in a graded fashion, while the lOFC has been proposed to encode specific sensory features of outcomes. The lOFC has also been proposed to encode stimulus outcome associations, which are then compared by value in the mOFC. Meta analysis of neuroimaging studies in humans reveals that a medial-lateral valence gradient exists, with the medial OFC responding most often to reward, and the lateral OFC responding most often to punishment. A posterior-anterior abstractness gradient was also found, with the posterior OFC responding to more simple reward, and the anterior OFC responding more to abstract rewards. Similar results were reported in a meta analysis of studies on primary versus secondary rewards.

[...]

The mid-anterior OFC has been found to consistently track subjective pleasure in neuroimaging studies. A hedonic hotspot has been discovered in the anterior OFC, which is capable of enhancing liking response to sucrose. The OFC is also capable of biasing the affective responses induced by α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) antagonism in the nucleus accumbens towards appetitive responses.





https://pubmed.ncbi.nlm.nih.gov/22145873/

In contrast, neurons in the OFC, but not the ACC, encode the value of a choice relative to the recent history of choice values. Together, these results suggest complementary valuation processes: OFC neurons dynamically evaluate current choices relative to the value contexts recently experienced, while ACC neurons encode choice predictions and prediction errors using a common valuation currency reflecting the integration of multiple decision parameters.





https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2693075/

Humans and other animals change their behavior in response to unexpected outcomes. The orbitofrontal cortex (OFC) is implicated in such adaptive responding, based on evidence from reversal tasks. Yet these tasks confound using information about expected outcomes with learning when those expectations are violated. OFC is critical for the former function; here we show it is also critical for the latter. In a Pavlovian over-expectation task, inactivation of OFC prevented learning driven by unexpected outcomes, even when performance was assessed later. We propose this reflects a critical contribution of outcome signaling by OFC to encoding of reward prediction errors elsewhere. In accord with this proposal, we report that signaling of reward predictions by OFC neurons was related to signaling of prediction errors by dopamine neurons in ventral tegmental area (VTA). Furthermore, bilateral inactivation of VTA or contralateral inactivation of VTA and OFC disrupted learning driven by unexpected outcomes.





https://link.springer.com/article/10...429-015-1139-z

Left medial orbitofrontal cortex volume correlates with skydive-elicited euphoric experience

The medial orbitofrontal cortex has been linked to the experience of positive affect. Greater medial orbitofrontal cortex volume is associated with greater expression of positive affect and reduced medial orbital frontal cortex volume is associated with blunted positive affect. However, little is known about the experience of euphoria, or extreme joy, and how this state may relate to variability in medial orbitofrontal cortex structure. To test the hypothesis that variability in euphoric experience correlates with the volume of the medial orbitofrontal cortex, we measured individuals’ (N = 31) level of self-reported euphoria in response to a highly anticipated first time skydive and measured orbitofrontal cortical volumes with structural magnetic resonance imaging. Skydiving elicited a large increase in self-reported euphoria. Participants’ euphoric experience was predicted by the volume of their left medial orbitofrontal cortex such that, the greater the volume, the greater the euphoria. Further analyses indicated that the left medial orbitofrontal cortex and amygdalo-hippocampal complex independently explain variability in euphoric experience and that medial orbitofrontal cortex volume, in conjunction with other structures within the mOFC-centered corticolimbic circuit, can be used to predict individuals’ euphoric experience.





https://psu.pb.unizin.org/psych425/c...and-the-brain/

One study (Coccaro et al., 2007) compared control participants to participants diagnosed with intermittent explosive disorder (IED), a disorder defined by overly aggressive behaviors. While an fMRI scanned their brain, participants viewed seven of Ekman’s FACS emotional expressions and clicked a button to indicate the gender of the individual in the photo. Results showed that when participants viewed only the ANGRY faces, IED participants exhibited greater activity in the amygdala, but less activity in the orbitofrontal cortex (OFC), compared to control participants. Does this show anger results in an overactive amygdala and underactive OFC? Maybe! But consider which emotions participants may have been experiencing when viewing the ANGRY face.

[...]

Studies on normal populations have shown that as the OFC shows greater activation to angry faces, people exhibit reduced aggressive behavior (Beyer et al, 2015). These findings would suggest that for normal functioning individuals, when we experience anger, the OFC helps us to regulate our aggressive approach behaviors.





https://pubmed.ncbi.nlm.nih.gov/15134840/

The orbitofrontal cortex contains the secondary taste cortex, in which the reward value of taste is represented. It also contains the secondary and tertiary olfactory cortical areas, in which information about the identity and also about the reward value of odours is represented. The orbitofrontal cortex also receives information about the sight of objects from the temporal lobe cortical visual areas, and neurons in it learn and reverse the visual stimulus to which they respond when the association of the visual stimulus with a primary reinforcing stimulus (such as taste) is reversed. This is an example of stimulus-reinforcement association learning, and is a type of stimulus-stimulus association learning. More generally, the stimulus might be a visual or olfactory stimulus, and the primary (unlearned) positive or negative reinforcer a taste or touch. A somatosensory input is revealed by neurons that respond to the texture of food in the mouth, including a population that responds to the mouth feel of fat. In complementary neuroimaging studies in humans, it is being found that areas of the orbitofrontal cortex are activated by pleasant touch, by painful touch, by taste, by smell, and by more abstract reinforcers such as winning or losing money. Damage to the orbitofrontal cortex can impair the learning and reversal of stimulus-reinforcement associations, and thus the correction of behavioural responses when there are no longer appropriate because previous reinforcement contingencies change. The information which reaches the orbitofrontal cortex for these functions includes information about faces, and damage to the orbitofrontal cortex can impair face (and voice) expression identification. This evidence thus shows that the orbitofrontal cortex is involved in decoding and representing some primary reinforcers such as taste and touch; in learning and reversing associations of visual and other stimuli to these primary reinforcers; and in controlling and correcting reward-related and punishment-related behavior, and thus in emotion. The approach described here is aimed at providing a fundamental understanding of how the orbitofrontal cortex actually functions, and thus in how it is involved in motivational behavior such as feeding and drinking, in emotional behavior, and in social behavior.





https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8789785/

Feeling disgusted was specifically correlated with increased activity in the insula, the basal ganglia, and frontal brain regions, such as the dorsolateral prefrontal cortex (DLPFC) and orbitofrontal cortex (OFC).





https://www.ucsf.edu/news/2023/05/42...e-chronic-pain

The ACC has long been implicated in the emotional dimension of pain and is associated with that basic feeling of “unpleasantness.” The OFC, which isn’t as well studied, has physical connections to the ACC and growing evidence suggests that it is activated in the cognitive dimension of pain — specifically the expectation of pain and its perceived intensity.

The study participants went about their daily lives for several months and reported pain scores about three times a day that described their pain severity and how it was making them feel in that moment. Immediately after jotting down the reports, they used a remote control to record 30 seconds of neural activity from the device implanted in their brains.

Using machine learning models, the researchers were able to predict the reported pain levels with specific neural activity patterns in each patient, defining a unique neural signature for that person’s pain experience. They found that signals from the OFC were more strongly correlated with episodes of chronic pain than those from the ACC.





https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5390724/

Pleasurable stimuli, including reward, inhibit pain, but the level of the neuraxis at which they do so and the cerebral processes involved are unknown. Here, we characterized a brain circuitry mediating pain inhibition by reward. Twenty-four healthy participants underwent functional magnetic resonance imaging while playing a wheel of fortune game with simultaneous thermal pain stimuli and monetary wins or losses. As expected, winning decreased pain perception compared to losing. Inter-individual differences in pain modulation by monetary wins relative to losses correlated with activation in the medial orbitofrontal cortex (mOFC). When pain and reward occured simultaneously, mOFCs functional connectivity changed: the signal time course in the mOFC condition-dependent correlated negatively with the signal time courses in the rostral anterior insula, anterior-dorsal cingulate cortex and primary somatosensory cortex, which might signify moment-to-moment down-regulation of these regions by the mOFC. Monetary wins and losses did not change the magnitude of pain-related activation, including in regions that code perceived pain intensity when nociceptive input varies and/or receive direct nociceptive input. Pain inhibition by reward appears to involve brain regions not typically involved in nociceptive intensity coding but likely mediate changes in the significance and/or value of pain.





https://www.sciencedirect.com/topics...frontal-cortex

The orbitofrontal cortex cytoarchitectonic areas of the human brain are shown in Fig. 1.3 (left). The medial orbitofrontal cortex includes areas 13 and 11 (Öngür et al., 2003). The lateral orbitofrontal cortex includes area 12 (sometimes in humans termed 12/47). The anterior cingulate cortex includes the parts shown in Fig. 1.3 (right) of areas 32, 25 (subgenual cingulate), and 24. The ventromedial prefrontal cortex includes areas 14 (gyrus rectus), 10 m, and 10r.

Some of the main connections of the orbitofrontal cortex in primates are shown schematically in Fig. 1.2 (Carmichael and Price, 1994, 1995; Barbas, 1995, 2007; Petrides and Pandya, 1995; Pandya and Yeterian, 1996; Ongür and Price, 2000; Price, 2006, 2007; Saleem et al., 2008, 2014; Mackey and Petrides, 2010; Petrides et al., 2012; Henssen et al., 2016; Rolls, 2017, 2019b,c; Rolls et al., 2020b). The orbitofrontal cortex receives inputs from the ends of every ventral cortical stream that processes the identity of visual, taste, olfactory, somatosensory, and auditory stimuli (Rolls, 2019b, 2021a). The ends of these cortical-processing streams provide a representation of the identity of the stimulus, independent of its reward value. This is shown by neuronal recordings in primates (Rolls, 2019b). For example, the inferior temporal cortex represents objects and faces independent of their reward value, as shown by visual discrimination reversal and devaluation of reward tests employing feeding to satiety (Rolls et al., 1977, 2020b; Rolls, 2012a, 2016a, 2019b, 2021a). Similarly, the insular primary taste cortex represents what the taste is independent of its reward value (Yaxley et al., 1988; Rolls, 2015b, 2016b, 2019b).

Outputs of the orbitofrontal cortex reach the anterior cingulate cortex (Rolls, 2019a), the striatum, the insula, and the inferior frontal gyrus and enable the reward value representations in the orbitofrontal cortex to influence behavior (Fig. 1.2, green). The orbitofrontal cortex projects reward value information to the anterior cingulate cortex, where that information generates the reward outcomes for action–outcome learning (Rushworth et al., 2012; Rolls, 2019a,b). The orbitofrontal cortex projects reward-related information to the ventral striatum (Williams et al., 1993), and this provides a route, in part via the habenula, for reward-related information to reach midbrain dopamine neurons (Rolls, 2017), which respond inter alia to positive reward prediction error (Bromberg-Martin et al., 2010; Schultz, 2016a). The basal ganglia support stimulus–response, habit learning (Everitt and Robbins, 2013; Rolls, 2014). Dopaminergic activity signals reward prediction error in the process of reinforcement learning (Schultz, 2016b; Cox and Witten, 2019). As the basal ganglia system depends upon dopamine in reinforcement learning of stimulus–response habits, it learns much more slowly than the orbitofrontal cortex (outcome)–anterior cingulate cortex (action) system for action–outcome goal-based learning, and for emotion (Rolls, 2021a). The orbitofrontal cortex projects to the viscero-autonomic cortex in the anteroventral insula (Hassanpour et al., 2018). Autonomic output helps to account for insular engagement in some emotion-related tasks in which the orbitofrontal cortex is involved (Rolls, 2016b, 2019b). The orbitofrontal cortex also projects to the inferior frontal gyrus, a region that on the right is implicated in stopping behavior and which, if damaged, can lead to impulsivity (Aron et al., 2014; Dalley and Robbins, 2017).





https://link.springer.com/referencew...7-79061-9_1462

Impulse control, or the ability to resist a drive to perform an action, is an ability that develops over time in an individual. The factors contributing to the development of impulse control are complex and involve multiple domains including biological, developmental, psychological, and cultural factors. The biological/anatomical aspects of the development of impulse control primarily relate to the development of specific brain structures. The cortical regions of the brain, generally the prefrontal cortex and more specifically the orbitofrontal cortex (OFC), are thought to be responsible for regulation of impulse control.





https://academic.oup.com/book/8333/c...dFrom=fulltext

The role of lateral orbitofrontal cortex in the inhibitory control of emotion

This chapter reviews neuropsychological, psychophysiological, and neuroimaging evidence that the lateral orbitofrontal cortex and ventrolateral prefrontal cortex regulates behavior by inhibiting the influence of a broad scope of sensations, feelings, thoughts, and actions. It is argued that the region facilitates successful goal-oriented behavior by inhibiting the influence of emotional feelings or perceptions. Such inhibitory processes are described in the context of physical sensation, including painful sensation, selective attention, emotion regulation, control of mood congruent biases, attitude regulation, memory, decision-making, and regulation in social interactions. This research is consistent with evidence showing that the lateral orbital/ventrolateral prefrontal governs the inhibition of habitual motor responses. The data are discussed with regard to dynamic filtering and disruption theory models of prefrontal functioning.





https://www.frontiersin.org/journals...016.00244/full

The orbitofrontal cortex (OFC) is involved in cognitive functions, and is also closely related to autonomic functions. The OFC is densely connected with the hypothalamus, a heterogeneous structure controlling autonomic functions that can be divided into two major parts: the lateral and the medial. Resting-state functional connectivity has allowed us to parcellate the cerebral cortex into putative functional areas based on the changes in the spatial pattern of connectivity in the cerebral cortex when a seed point is moved from one voxel to another. In the present high spatial-resolution fMRI study, we investigate the connectivity-based organization of the OFC with reference to the hypothalamus. The OFC was parcellated using resting-state functional connectivity in an individual subject approach, and then the functional connectivity was examined between the parcellated areas in the OFC and the lateral/medial hypothalamus. We found a functional double dissociation in the OFC: the lateral OFC (the lateral orbital gyrus) was more likely connected with the lateral hypothalamus, whereas the medial OFC (the medial orbital and rectal gyri) was more likely connected with the medial hypothalamus. These results demonstrate the fundamental heterogeneity of the OFC, and suggest a potential neural basis of the OFC–hypothalamic functional interaction.





https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2693075/

Humans and other animals change their behavior in response to unexpected outcomes. The orbitofrontal cortex (OFC) is implicated in such adaptive responding, based on evidence from reversal tasks. Yet these tasks confound using information about expected outcomes with learning when those expectations are violated. OFC is critical for the former function; here we show it is also critical for the latter. In a Pavlovian over-expectation task, inactivation of OFC prevented learning driven by unexpected outcomes, even when performance was assessed later. We propose this reflects a critical contribution of outcome signaling by OFC to encoding of reward prediction errors elsewhere. In accord with this proposal, we report that signaling of reward predictions by OFC neurons was related to signaling of prediction errors by dopamine neurons in ventral tegmental area (VTA). Furthermore, bilateral inactivation of VTA or contralateral inactivation of VTA and OFC disrupted learning driven by unexpected outcomes.





https://www.frontiersin.org/journals...017.00025/full

Structurally, both the OFC and the tightly functionally connected sgACC ...





https://www.sciencedirect.com/scienc...66432810003050

Decision neuroscience suggests that there exists a core network for the subjective valuation of rewards from a range of different domains, encompassing the ventral striatum and regions of the orbitofrontal cortex (OFC), in particular the ventromedial aspect of the OFC. Here we first review ways to measure subjective value experimentally in a cognitive neuroscience context, and provide a brief overview over different types of value (outcome, goal and decision value). We then compare results of functional neuroimaging studies of subjective value representations across these different types of value. Our analysis suggests that the same region of the mOFC represents the outcome values of primary reinforcers, but also more complex decision values in which multiple dimensions of the reward need to be integrated. The subjective (hedonic) experience of processing highly valued decision options (regardless of whether they refer to actually experienced rewards or merely potential future rewards) appears to be what is reflected in value-related mOFC activity.





https://www.researchgate.net/figure/...fig2_317629651

Contributions of medial OFC to emotion (A). Schematic overview of relevant anatomical inputs to medial OFC, based on anatomical connectivity findings. mOFC medial orbitofrontal cortex; RLPFC rostrolateral prefrontal cortex; RMPFC rostromedial prefrontal cortex; pgACC pregenual anterior cingulate cortex; hippo hippocampus; RSC retrosplenial cortex (B). From left to right: activation in medial OFC exhibits a positive correlation with the anticipated pleasantness of future scenarios involving combinations of familiar people and places, from Benoit et al. (2014); conjunction effect showing overlapping medial OFC activation for real monetary rewards and imagined rewarding scenarios, from Bray et al. (2010); medial OFC activation is stronger when participants imagined positive and negative events in the future relative to routine events, and this contrast was more pronounced for events imagined in the far future relative to the near future, from D'Argembeau et al. (2008); medial OFC activation parametrically increases with the reported pleasantness of recalled autobiographical memories, from Lin et al. (2016). See the online article for the color version of this figure.

https://i.imgur.com/XegbQeQ.png





https://www.researchgate.net/figure/...fig1_317629651

Contributions of lateral OFC to emotion (A). Schematic overview of relevant anatomical inputs to lateral OFC, based on anatomical connectivity findings. Not shown: connections with pyriform (olfactory) cortex and auditory cortex. lOFC lateral orbitofrontal cortex; RLPFC rostrolateral prefrontal cortex; ins/operc insula/frontal operculum; ITC inferotemporal cortex; DMPFC dorsomedial prefrontal cortex; S1 primary somatosensory cortex; FEFs frontal eye fields (B). Task design and results from Morrison and Salzman (2009). Monkeys viewed a visual cue that predicted the subsequent occurrence of one of three outcomes: large reward, small reward, or an aversive air puff. An example "appetitive" neuron shows the greatest increase in activity in response to the cue that predicts the large reward, and diminishing activity for the other two outcomes, whereas an example "aversive" neuron shows the reverse pattern. Thus, OFC neurons carry information about the value of the outcomes associated with the visual stimuli.

https://i.imgur.com/nJtz5Ou.png





https://academic.oup.com/braincomms/...caa196/5976759

https://i.imgur.com/psZ4raX.jpg





https://www.researchgate.net/figure/...fig1_359943987

https://i.imgur.com/cjgQNxS.jpg





https://i.imgur.com/82iA7jh.png

[Petter]

(see post #441 and #443)



https://en.wikipedia.org/wiki/Anterior_cingulate_cortex

The most basic form of ACC theory states that the ACC is involved with error detection. Evidence has been derived from studies involving a Stroop task. However, ACC is also active during correct response, and this has been shown using a letter task, whereby participants had to respond to the letter X after an A was presented and ignore all other letter combinations with some letters more competitive than others. They found that for more competitive stimuli ACC activation was greater.

A similar theory poses that the ACC's primary function is the monitoring of conflict. In Eriksen flanker task, incompatible trials produce the most conflict and the most activation by the ACC. Upon detection of a conflict, the ACC then provides cues to other areas in the brain to cope with the conflicting control systems.

[...]

A more comprehensive and recent theory describes the ACC as a more active component and poses that it detects and monitors errors, evaluates the degree of the error, and then suggests an appropriate form of action to be implemented by the motor system. Earlier evidence from electrical studies indicate the ACC has an evaluative component, which is indeed confirmed by fMRI studies. The dorsal and rostral areas of the ACC both seem to be affected by rewards and losses associated with errors. During one study, participants received monetary rewards and losses for correct and incorrect responses, respectively.

[...]

The ACC is the cortical area that has been most frequently linked to the experience of pain. It appears to be involved in the emotional reaction to pain rather than to the perception of pain itself.

[...]

In The Astonishing Hypothesis, Francis Crick identifies the anterior cingulate, to be specific the anterior cingulate sulcus, as a likely candidate for the center of free will in humans.





https://www.hrplab.org/notes-functio...etic-approach/

https://en.wikipedia.org/wiki/Salience_network

The salience network [...] is a large scale network of the human brain that is primarily composed of the anterior insula (AI) and dorsal anterior cingulate cortex (dACC). It is involved in detecting and filtering salient stimuli, as well as in recruiting relevant functional networks. Together with its interconnected brain networks, the SN contributes to a variety of complex functions, including communication, social behavior, and self-awareness through the integration of sensory, emotional, and cognitive information.





https://en.wikipedia.org/wiki/Von_Economo_neuron

Von Economo neurons are found in two very restricted regions in the brains of hominids (humans and other great apes): the anterior cingulate cortex (ACC) and the fronto-insular cortex (FI) (which each make up the salience network). In 2008, they were also found in the dorsolateral prefrontal cortex of humans. Von Economo neurons are also found in the brains of a number of cetaceans, African and Asian elephants, and to a lesser extent in macaque monkeys and raccoons. The appearance of von Economo neurons in distantly related clades suggests that they represent convergent evolution – specifically, as an adaptation to accommodate the increasing size of these distantly-related animals' brains.





https://isfassociates.com/unlocking-...gulate-cortex/

One of the most intriguing aspects of the pgACC is its involvement in emotional regulation. Emotional regulation refers to our ability to manage and modulate our emotions effectively. This means being able to understand, express, and cope with our feelings in a way that promotes well-being and adaptive behavior. A well-regulated pgACC will help the individual not overly identify with their emotional states, allowing them to identify, tolerate and move through more uncomfortable types of emotions. This allows the individual to identify “I am feeling sad”, rather than “I am sadness”, and allows them to recruit other networks, such as the salience network, to help process this emotional state and identify what’s important in knowing how to move through feeling sad.

Research has shown that the pgACC plays a key role in assessing the emotional significance of stimuli from both external and internal sources. It helps us recognize emotional cues in others and ourselves, allowing us to empathize and respond appropriately. Additionally, the pgACC is essential in mediating the experience of empathy, compassion, and social connectedness, all of which are crucial for emotional well-being.





https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6875144/

In humans, the pregenual anterior cingulate cortex receives information related to reward from the medial orbitofrontal cortex, and related to punishment and not receiving reward from the lateral orbitofrontal cortex. These orbitofrontal cortex areas represent information about value, not about actions or responses, as shown by neuronal recordings in macaques. The value representation received by the anterior cingulate cortex includes information about the outcome of actions, that is, whether reward or punishment has been received, and is used by the cingulate cortex for learning the action to perform to obtain a reward or avoid a punisher. This is termed ‘action–outcome learning’. The anterior cingulate cortex is implicated in emotion, because it is involved in linking reward and punishment information, which elicit emotional responses, to behaviour, and, in particular, to actions. The subgenual cingulate cortex (area 25) may link rewards and punishers to autonomic output. The posterior cingulate cortex receives information about actions from the parietal cortex, including areas 7a, VIP and LIP laterally, and area 7m medially (as well as some inputs from ventral stream temporal lobe areas) (Vogt and Laureys 2009). The posterior cingulate cortex is therefore implicated in spatial including visuospatial processing. A concept is that the posterior cingulate action-related information is brought together with the anterior cingulate cortex outcome-related information, and via the midcingulate cortex the result of action–outcome learning can influence premotor areas that receive information from the midcingulate cortex (Fig. 1). The posterior cingulate cortex in addition has major connectivity with parahippocampal areas TF and TH, which in turn project spatial information to the entorhinal cortex and thereby into the hippocampal episodic memory system. The posterior cingulate cortex provides a route for spatial including visuospatial information to reach the hippocampus, where it can be combined with object and reward-related information to form episodic memories (Rolls 2016a, 2018b; Rolls and Wirth 2018). The posterior cingulate cortex is thereby also implicated in memory.





https://www.sciencedirect.com/topics...ngulate-cortex

The orbitofrontal cortex projects to the pregenual cingulate cortex (Carmichael & Price, 1996; Price, 2006), and both these areas have reward and punishment value representations that correlate on a continuous scale with the subjective pleasantness/unpleasantness ratings of olfactory (Anderson et al., 2003; Grabenhorst et al., 2007; Rolls, Critchley, Mason, et al., 1996; Rolls, Kringelbach, et al., 2003), taste (Grabenhorst, Rolls, & Bilderbeck, 2008; Rolls, 2008b; Rolls, Sienkiewicz, et al., 1989; Small et al., 2003), somatosensory (Rolls, O'Doherty, et al., 2003), temperature (Guest et al., 2007), visual (O'Doherty et al., 2003), monetary (Knutson, Rick, Wimmer, Prelec, & Loewenstein, 2007; O'Doherty, Kringelbach, et al., 2001), and social stimuli (Hornak et al., 2003; Kringelbach & Rolls, 2003; Moll et al., 2006; Spitzer, Fischbacher, Herrnberger, Gron, & Fehr, 2007) (see further Bush, Luu, & Posner, 2000; Grabenhorst & Rolls, 2011; Rolls, 2009a, 2014). Indeed, the pregenual cingulate cortex may be identified inter alia as a tertiary cortical taste area, with single neurons responding to the taste and texture of food (Rolls, 2008b). Moreover, there is very interesting topology, with the activations that are correlated with the pleasantness of stimuli in the pregenual cingulate cortex, and the activations that are correlated with the unpleasantness of stimuli just dorsal and posterior to this, extending back above the genu of the corpus callosum (Grabenhorst & Rolls, 2011; Rolls, 2014).

We may ask why, if the activations in the orbitofrontal cortex and the pregenual cingulate cortex are somewhat similar in their continuous and typically linear representations of reward or affective value (pleasantness ratings), are there these two different areas? A suggestion I make (Rolls, 2014) is that the orbitofrontal cortex is the region that computes the rewards, expected rewards etc., and updates these rapidly when the reinforcement contingencies change, based on its inputs about primary reinforcers from the primary taste cortex (Baylis et al., 1995), the primary olfactory cortex (Carmichael et al., 1994), the somatosensory cortex (Morecraft et al., 1992), etc. The orbitofrontal cortex makes explicit in its representations the reward value, based on these inputs, and in a situation where reward value is not represented at the previous tier, but instead where the representation is about the physical properties of the stimuli, their intensity, etc. (Grabenhorst & Rolls, 2008; Grabenhorst, Rolls, & Bilderbeck, 2008; Grabenhorst et al., 2007; Rolls, 2014; Rolls, Grabenhorst, & Parris, 2008; Rolls, O'Doherty, et al., 2003; Small et al., 2003) (see Fig. 1). The orbitofrontal cortex computes the expected value of previously neutral stimuli, and updates these representations rapidly when the reinforcement contingencies change, as described here. Thus the orbitofrontal cortex is the computer of reward magnitude and expected reward value. It can thus represent outcomes, and expected outcomes, but it does not represent actions such as motor responses or movements (Rolls, 2014). It is suggested that the representations of outcomes, and expected outcomes, are projected from the orbitofrontal cortex to the pregenual cingulate cortex, as the cingulate cortex has longitudinal connections which allow this outcome information to be linked to the information about actions that is represented in the midcingulate cortex, and that the outcome information derived from the orbitofrontal cortex can contribute to action–outcome learning implemented in the cingulate cortex (Rolls, 2008c, 2014; Rushworth, Behrens, Rudebeck, & Walton, 2007; Rushworth, Buckley, Behrens, Walton, & Bannerman, 2007; Rushworth, Noonan, Boorman, Walton, & Behrens, 2011). Some of this evidence on action–outcome learning has been obtained in rat lesion studies, and indicates that the costs of actions, as well as the rewards produced by actions, involve the ACC. Although the ACC is activated in relation to autonomic function (Critchley, Wiens, Rotshtein, Ohman, & Dolan, 2004), its functions clearly extend much beyond this, as shown also for example by the emotional changes that follow damage to the ACC and related areas in humans (Hornak et al., 2003).

In responding when the reward obtained is less than that expected, the orbitofrontal cortex negative reward prediction error neurons are working in a domain that is related to the sensory inputs being received (expected reward and reward obtained). There are also error neurons in the ACC that respond when errors are made (Niki & Watanabe, 1979), or when rewards are reduced (Shima & Tanji, 1998) (and in similar imaging studies, Bush et al., 2002). Some of these neurons may be influenced by the projections from the orbitofrontal cortex, and reflect a mismatch between the reward expected and the reward that is obtained. However, some error neurons in the ACC may reflect errors that arise when particular behavioural responses or actions are in error, and this type of error may be important in helping an action system to correct itself, rather than, as in the orbitofrontal cortex, when a reward prediction system about stimuli needs to be corrected. Consistent with this, many studies provide evidence that errors made in many tasks activate the anterior/midcingulate cortex, whereas tasks with response conflict activate the superior frontal gyrus (Matsumoto, Matsumoto, Abe, & Tanaka, 2007; Rushworth & Behrens, 2008; Rushworth, Walton, Kennerley, & Bannerman, 2004; Vogt, 2009).

A neuroimaging study in humans illustrates how non-reward/error signals relevant to emotion and social behaviour are found in the ACC. Kringelbach et al. (2003) used the faces of two different people, and if one face was selected then that face smiled, and if the other was selected, the face showed an angry expression. After good performance was acquired, there were repeated reversals of the visual discrimination task. Kringelbach et al. (2003) found that activation of a lateral part of the orbitofrontal cortex and in a dorsal part of the ACC in the fMRI study was produced on the error trials, that is when the human chose a face, and did not obtain the expected reward. An interesting aspect of this study that makes it relevant to human social behaviour is that the conditioned stimuli were faces of different individuals, and the USs were face expressions. Thus the association that was being reversed in this study was between a representation of face identity and a representation of face expression. Moreover, the study reveals that the human orbitofrontal cortex and ACC are very sensitive to social feedback when it must be used to change behaviour (Kringelbach & Rolls, 2003, 2004).





https://www.nature.com/articles/s41598-021-89405-y

Neurobiological models of emotion focus traditionally on limbic/paralimbic regions as neural substrates of emotion generation, and insular cortex (in conjunction with isocortical anterior cingulate cortex, ACC) as the neural substrate of feelings.





https://en.wikipedia.org/wiki/Feeling

The neuroscientist Antonio Damasio distinguishes between emotions and feelings: Emotions are mental images (i.e. representing either internal or external states of reality) and the bodily changes accompanying them, whereas feelings are the perception of bodily changes. In other words, emotions contain a subjective element and a 3rd person observable element, whereas feelings are subjective and private.





https://dakotafamilyservices.org/res...ings-emotions/

Emotions

Emotions, which originate as sensations in the body, are intense feelings (exhilaration, terror, despair) that last only seconds to minutes. They are controlled by chemicals our brains release in response to a trigger or event—basically our body's response to whatever is happening around us. The chemicals go throughout our body, forming a feedback loop between our body and brain, creating emotion.

Emotions are always based on an external stimulus, and almost always come and subside quickly. In addition to being specific and a reaction to something, emotions have corresponding and universal facial expressions and body language.




Feelings

While emotions start as sensations in the body, feelings are generated from our thoughts about those emotions. Or in other words, feelings are how we interpret emotions and let them sink in.

We use the word, "feel," for both physical and emotional states. For instance, we can "feel cold" both physically and emotionally. Feelings can be diluted or distorted by the stories we've unconsciously created based on past events or experiences.




Moods

A mood is a state of mind or a general feeling that can influence your thoughts, behaviors, and actions. Moods tend to be less intense than emotions and do not necessarily depend on an event or trigger. Rather than being how you feel in each moment, your mood is how you feel over time.

Moods are influenced by the environment, diet, exercise, physical health, and what you choose to think about. They can last minutes, hours, or days, and they have no unique corresponding nonverbal facial expressions or body language.

[Petter]

(see post #450)


https://www.sciencedirect.com/scienc...49763423000799

Frustration (“goal-blockage”) is a special case of aversive stimulus-response situations. The Frustration-Aggression hypothesis began as an explanation of all human aggression (Dollard et al., 1939). Now reduced in scope, it remains a focus in road rage studies. It has also morphed into operant schedule-induced, aggression-motivating “frustrative non-reward” demonstrated in fish, birds and mammals (Coppens et al., 2014, David et al., 2004, Looney and Cohen, 1982).





https://psu.pb.unizin.org/psych425/chapter/not-every-frustration-causes-anger/

In conclusion, this study shows us that simply experiencing a frustration does not result in overt aggression. Instead, experiencing a frustration that is deliberately caused by another causes the most aggression.





https://www.sciencedirect.com/scienc...28009352000117

The Neural Basis of Frustration State

From missing the bus to helplessly observing someone procure our taxi, daily life throws numerous obstacles in the path of our desired goals. Mammalian studies show that frustration is experienced when goal-directed activity is blocked. Using a newly developed multitrial reward schedule task combined with functional magnetic resonance imaging (fMRI), we show that both proximity and expended effort modulated brain responses to blocked reward in regions implicated in animal models of reactive aggression, including the amygdala, midbrain periaqueductal gray (PAG), insula, and prefrontal cortex. These findings suggest that frustration may serve an energizing function, translating unfulfilled motivation into aggressive-like surges via a cortical, amygdala, and PAG network. These studies may enhance our understanding of the neuropsychological mechanisms of the frustration state and frustration-related mental disorders, such as pathological aggression.





https://www.frontiersin.org/journals...015.01989/full

Effect of Frustration on Brain Activation Pattern in Subjects with Different Temperament

The most consistent stress-related results from MIST studies indicate decreased activity in parts of the limbic system: hippocampus, medio-orbitofrontal cortex (mOFC) and ACC (Pruessner et al., 2010) and increased dopamine release in ventral striatum and basal ganglia (Pruessner et al., 2004; Soliman et al., 2008; Dedovic et al., 2009).

To the best of our knowledge there have been so far only two fMRI studies explicitly dealing with frustration. In the first experiment the authors defined frustration as an emotional component of processing the omission of a desired goal (Abler et al., 2005). The experiment consisted of the series of easy tasks. After each series the participants could either or get nothing. The results revealed a decrease in ventral striatum activity and an increase in RVPFC and right insula in the reward omission condition. In the second study (Yu et al., 2014) authors developed a procedure in which expected reward was blocked and levels of experienced frustration were parametrically varied by manipulating the participants’ motivation to obtain the reward prior to blocking. The activations associated with frustration were observed in amygdala, midbrain periaqueductal gray (PAG), insula, and prefrontal cortex. However, the authors of this study were interested mostly in frustration that leads to reactive aggression.

[Petter]

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5846103/

There is increasing evidence that the kappa-opiate receptor, in addition to the mu-opiate receptor, plays an important role in substance use pathophysiology and behavior. As dopamine activity is upregulated through chronic substance use, kappa receptor activity, mediated through the peptide dynorphin, is upregulated in parallel. Dynorphin causes dysphoria and decreased locomotion, and the upregulation of its activity on the kappa receptor likely dampens the excitation caused by increased dopaminergic activity. This feedback mechanism may have significant clinical implications for treating drug dependent patients in various stages of their pathology.





https://en.wikipedia.org/wiki/Dynorphin

Land et al. first described a mechanism of dysphoria in which corticotropin-releasing factor (CRF) provokes dynorphin release. While control mice displayed aversive behaviors in response to forced swim tests and foot shocks, mice lacking dynorphin did not show any such signs of aversion. They noted that injecting CRF led to aversive behaviors in mice with functional genes for dynorphin even in the absence of stress, but not in those with dynorphin gene deletions. Place aversion was eliminated when the receptor CRF2 was blocked with an antagonist.





https://en.wikipedia.org/wiki/%CE%9A-opioid_receptor

Similarly to μ-opioid receptor (MOR) agonists, KOR agonists are potently analgesic, and have been employed clinically in the treatment of pain. However, KOR agonists also produce side effects such as dysphoria, hallucinations, and dissociation, which has limited their clinical usefulness.

[Petter]

https://en.wikipedia.org/wiki/Acetylcholine

In addition, ACh acts as an important internal transmitter in the striatum, which is part of the basal ganglia. It is released by cholinergic interneurons. In humans, non-human primates and rodents, these interneurons respond to salient environmental stimuli with responses that are temporally aligned with the responses of dopaminergic neurons of the substantia nigra.

------

noradrenaline <--> anger/arousal + aggression

acetylcholine <--> anger/arousal (frustration)

[Petter]

"Hostility is inhibited by serotonin, while acetylcholine may be the trigger for anger, as the abilities of cholinergic drugs to elicit rage in cats and of cholinergic blockers to decrease marital conflict illustrate. Anger and depression (Freud's anger turned inward) may share the same chemical modulation. [...] Thus, depression and anger might be both triggered by acetylcholine and inhibited by serotonin."

https://i.imgur.com/swMN3zY.png

https://en.wikipedia.org/wiki/Substance_P

Substance P and the NK1-receptor are widely distributed in the brain and are found in brain regions that are specific to regulating emotion (hypothalamus, amygdala, and the periaqueductal gray). They are found in close association with serotonin (5-HT) and neurons containing norepinephrine that are targeted by the currently used antidepressant drugs.

[Petter]

https://i.imgur.com/j2sNxel.jpg





https://i.imgur.com/4EnMgra.jpg





https://www.researchgate.net/figure/..._fig4_41423098

A potential role of the habenula (HB) in the reward system. The ventral tegmental area (VTA)–nucleus accumbens (NAc) pathway plays a critical role in reward. Dopaminergic projections innervate the NAc. How much stimulation from the VTA reaches the NAc may be influenced by the HB, which signals to the VTA when no reward is expected. The NAc in turn feeds back to the HB, thereby establishing a regulatory circuit balancing dopamine levels in the brain.





https://www.researchgate.net/figure/Illustration-showing-the-interaction-of-at-least-seven-major-neurotransmitter-pathways-in_fig1_363143461





https://www.transpopmed.org/articles/tppm/tppm-2022-9-165.php





https://sites.tufts.edu/opioidpeptides/pathways-and-receptors/mu-receptors/

To summarize, in a sort of biological double-negative, µ opioid agonism in the VTA inhibits the inhibitory action of GABA on dopamine-releasing neurons, resulting in promotion of dopamine release to other neurons. Dopamine release causes the euphoric feeling, or “high,” experienced during opioid use.





https://en.wikipedia.org/wiki/Lateral_hypothalamus

Through the diverse outputs of the orexin system, the orexin neurons in the lateral hypothalamus mediate an array of functions. Two of the most commonly noted functions of orexin peptides in the lateral hypothalamus are the promotion of feeding behavior and arousal (i.e., wakefulness).





https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3629303/

The link between orexin and the ventral tegmental nucleus serves to motivate an animal to engage in goal-directed behavior.





https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8041470/

Early studies on the LHA demonstrated that electrical stimulation of this region profoundly increased food consumption, whereas LHA disruption resulted in dramatic under-consumption of food. Therefore, the LHA was initially characterized as a “feeding hotspot”. However, in addition to influencing energy intake, stimulation to this region also invigorated other motivated behaviors such as drinking, physical activity, and copulation.





https://www.scientificamerican.com/a...ncy-of-desire/

The researchers were puzzled. Instead of producing pleasure, dopamine seemed to drive desire.





https://www.psychologytoday.com/us/b...-food-cravings

While you may already know that dopamine, aka the “pleasure chemical,” functions as an important neurotransmitter, or messenger between neurons, you may not know that the release of dopamine in the brain often starts at the tongue.

Our tongue is an oasis of sensory receptors that absorb distinct flavor profiles, textures, and more. Our tongue’s taste buds act as a gateway that receives information from our food and translates it into both pleasurable and non-pleasurable signals. These signals suggest to our body which foods can either enhance or detract from our living experience.

Each of us has a pathway that connects the taste buds on our tongue to dopamine producing cells in our brain. This pathway is known as the gustatory system, and it is where pleasure from eating food starts. When we immerse our tongue in an experience with hyper-concentrated sugar, salt, or carbohydrates (i.e. hyperpalatable foods), dopamine levels surge in the part of our brain known as the nucleus accumbens. Furthermore, the greater the release of dopamine, the greater the sensation of pleasure. Ultimately, this is how we experience pleasure from food.





https://sites.lsa.umich.edu/berridge...oyful-mind.pdf

Wanting and liking are both involved in making an experience feel rewarding. So it makes sense that the real pleasure centers in the brain—those directly responsible for generating pleasurable sensations—turn out to lie within some of the structures previously identified as part of the reward circuit. One of these so-called hedonic hotspots lies in a subregion of the nucleus accumbens called the medial shell. A second is found within the ventral pallidum, a deep-seated structure near the base of the forebrain that receives most of its signals from the nucleus accumbens. To locate these hotspots, we searched for brain regions that, when stimulated, amplify the sensation of pleasure—for example, making sweet things even more enjoyable.

Chemically stimulating these hotspots with enkephalin—a morphinelike substance made in the brain—enhances a rat’s liking of sweets. Anandamide, the brain’s version of the active ingredient in marijuana, does the same. Another hormone called orexin, which is released by the brain during hunger, may also stimulate hedonic hotspots, helping to enhance the flavor of food. Each of these spots is just a fraction of the size of the larger structure in which it lies—only about one cubic millimeter in a rat brain and probably no more than a cubic centimeter in a human. Yet like the islands of an archipelago, they link to one another—and to other brain regions that process pleasure signals—to form a powerful, integrated pleasure circuit. That circuit is fairly resilient. In our experience, disabling individual components within the pleasure circuit does not diminish the typical response to a standard sweet—with one exception. Damaging the ventral pallidum appears to eliminate an animal’s ability to enjoy food, turning a nice taste nasty. On the other hand, intense euphoria is harder to come by than everyday pleasures. The reason may be that strong enhancement of pleasure—like the chemically induced pleasure bump we produced in lab animals—seems to require activation of the entire network at once. Defection of any single component dampens the high.

Whether the pleasure circuit—and in particular, the ventral pallidum—works the same way in humans is unclear. Not many people come to the clinic with discrete damage to these structures without injuries in surrounding areas. Thus, it is difficult to assess whether the ventral pallidum and other components in the circuit are essential to the sensation of pleasure in humans. We know of one patient whose ventral pallidum became damaged during a massive drug overdose. Afterward, he reported that his feelings were dominated by depression, hopelessness, guilt and an inability to feel pleasure—potentially supporting a central role for this heretofore underappreciated structure.





https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9897479/

Emerging evidence supports the notion that, in cooperation with the anterior cingulate cortex (Cg), the LHb participates in adjusting behaviors based on the expectation of outcomes.





https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5374329/

To understand the model, one needs to first appreciate some basic concepts relating to reward processing. Imagine a rat, walking through a maze for the first time, hoping to find food. When the rat finds food, dopamine neurons in the ventral tegmental area (VTA) have a burst of firing, releasing dopamine in the striatum and cortex. On subsequent runs through the same maze, a very different pattern emerges. As the rat becomes increasingly confident of where the reward will be, dopamine is released in conjunction with cues that will predict where and when the reward will be found rather than as a single burst when the rat finds the actual food (4). Two key points emerge from these studies. First, the dopamine burst can be seen not as indicating reward per se but rather as a learning signal about the environment (what just happened was important and good—remember how you got here!). Second, as the dopamine firing shifts forward to the predictive cues, the signal can again be seen to reflect not the reward itself but rather the expectation of future rewards.

Consider, now, a different scenario. After the rat has learned the maze, it returns to the same space, eager to claim its reward—only to discover that no food is present. In the same way that the VTA previously signaled the presence of an unexpected reward, now the lateral habenula fires—thereby signaling an unexpected setback (5). The firing of the lateral habenula activates intermediary inhibitory neurons that then suppress the VTA dopamine neurons (Figure 1). In this model, the lateral habenula is like Eeyore from A. A. Milne’s classic Winnie-the-Pooh stories—a vocal pessimist attuned to any possibility of misfortune.





https://www.ncbi.nlm.nih.gov/books/NBK424849/

Opioids attach to opioid receptors in the brain, which leads to a release of dopamine in the nucleus accumbens, causing euphoria (the high), drowsiness, and slowed breathing, as well as reduced pain signaling (which is why they are frequently prescribed as pain relievers).

[...]

Like other drugs, marijuana (also called cannabis) leads to increased dopamine in the basal ganglia, producing the pleasurable high.





https://www.nature.com/articles/1301376

These results provide the first demonstration that endocannabinoids in the nucleus accumbens specifically amplify the hedonic impact of a prototypical sensory pleasure, sweetness. Anandamide acted especially in a dorsal hotspot of medial shell in nucleus accumbens to enhance positive ‘liking’ reactions to a rewarding sucrose taste. It would be of interest to know whether other types of sensory pleasure besides sweetness can be enhanced by the endocannabinoid hedonic hotspot described here, and whether the rewarding and euphoric effects of exogenous cannabinoid drugs such as Δ9-THC are mediated by the same endocannabinoid hedonic hotspot that amplifies taste ‘liking’. Food intake was also stimulated by anandamide microinjections that amplified hedonic ‘liking’, suggesting that magnifying the pleasurable impact of food reward might be part of the mechanism for cannabinoid promotion of appetite or incentive motivation. Endocannabinoid hedonic hotspots for sensory pleasures may thus be important to understanding how the brain normally processes pleasurable natural rewards and generates incentive motivation. Dysfunction of endocannabinoid hedonic/motivational mechanisms highlighted here might also be relevant to understanding what goes awry in certain hedonic or appetitive disorders such as depression, drug addiction, and obesity.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4425246/

Resolving the cocaine puzzle? Another puzzle has been that if dopamine does not cause sensory pleasure, why are dopamine-promoting drugs such as cocaine or methamphetamine so pleasant? There are several potential answers, both psychological and neurobiological. A psychological explanation may be that at least some of the euphoria of cocaine or amphetamine drugs comes from a ‘wanting’ component of reward. That is, high incentive salience is just one component used to construct reward experiences (together with high hedonic impact). But on its own, elevated incentive salience induced by dopamine stimulation may to some extent be mistaken for pleasure itself. Drug enhancement of incentive salience could make other people, events or actions in the world all seem more attractive, and be powerfully enabling of engagement with them, which might well carry an aura of euphoria even if not truly hedonic. Viewed this way, subjective reward experience may be partly synthesized from motivation and cognitive appraisal components, similar to many other emotions (Barrett et al., 2007). This mistaken appraisal explanation may also apply to cases of electrode self-stimulation described below.

A neural explanation for why cocaine is pleasant may be that cocaine and amphetamine also stimulate secondary recruitment of endogenous opioid and related neurobiological hedonic mechanisms, beyond directly raising dopamine release. Those recruited secondary mechanisms may more directly cause ‘liking’ reactions and subjective pleasure. For instance, dopamine-stimulating drugs recruit elevation in nucleus accumbens of endogenous opioid and GABA signals (Colasanti et al., 2012; Soderman and Unterwald, 2009; Tritsch et al., 2012). Elevated endogenous opioid release in a site such as the NAc hedonic hotspot could amplify ‘liking’ as described above, resulting in a more genuinely pleasurable experience. Similarly, GABA signals in the far rostral strip of NAc shell can also enhance true ‘liking’ (Faure et al., 2010), which could occur if drugs of abuse that stimulate dopamine neurons also stimulate some of those neurons to co-release more GABA in NAc (Tritsch et al., 2012).

https://www.kringelbach.org/papers/P...giadis2012.pdf

Drugs of abuse that enhance sympathetic arousal also typically induce euphoria, which is described as intensely pleasurable, especially in drug naive participants (Vollm et al., 2004). In one fMRI study, participants rated feelings of high, low, rush, and craving after cocaine infusion (Breiter et al., 1997). Rush and high both peaked within 3 min after the volunteers received cocaine, after which these feelings dissipated (though rush more quickly than high). Because of the strong overlap in rush and high ratings, only rush was used as regressors in the brain activity analysis. Thus, areas correlating with rush are not only likely to reflect general arousal effects (e.g. elevated heart rate, sweating), but also the euphoria associated with high. The overlap between areas related to cocaine rush/high and sexual arousal (genital stimulation) is striking, and includes aMCC, anterior and posterior insula, ventral pallidum/basal forebrain, and frontal operculum/vPMC. In addition, the amygdala showed prolonged decreased activity after cocaine infusion, similar to decreased activity during sexual genital stimulation (Georgiadis et al., 2009, 2010a).

The VS/NAcc showed a predominant association with ratings of craving, but also active during peak rush (Breiter et al., 1997). Moreover, both VS/NAcc and OFC was active during a saline retest, which is suggestive of expectancy effects in these areas similar to those observed for sexual stimuli (Klucken et al., 2009; Sescousse et al., 2010).

------

excitement <--> he approaches a reward (or a goal) ..... lateral hypothalamus ---> VTA ---> NAcc

happiness (he gets excited easily) ..... OFC/ACC ---> habenula ---> VTA

euphoria 1 (intense feelings of happiness)

euphoria 2 (intense feelings of well-being/pleasure) ..... hedonic hotspots: NAcc and ventral pallidum

[Petter]

https://www.nature.com/articles/s41586-023-06492-9

Striatal dopamine and acetylcholine are essential for the selection and reinforcement of motor actions and decision-making.





https://www.researchgate.net/figure/...fig3_237121645





https://www.sciencedaily.com/release...0419131108.htm





https://insidescientific.com/fright-...-the-amygdala/

Dopamine, a neurotransmitter most popularly thought of as the “pleasure hormone,” has far greater roles in fear conditioning than previously thought. Fear conditioning is an evolutionarily-shaped mechanism responsible for aversive memory formation. This response to negative stimuli has been crucial for species survival, as it allows one to predict a negative event based on the association of a previously neutral cue with an aversive stimulus. These neurochemical linkings occur in the amygdala, a brain region that supports associative and emotional learning, and is also heavily innervated by dopamine.

[...]

Frick et al. demonstrated that human fear conditioning and learning strength is directly linked to endogenous dopamine release in the amygdala. These findings are consistent with previous rodent studies, indicating that this mechanism is evolutionarily conserved. The authors also found that while learning strength was linked to dopamine release, the strength of the unconditioned response was not, providing further evidence of dopamine’s role in learning-related processes. Previous studies have also reported that fear conditioning can induce a greater increase in dopamine concentration than an independent shock.





https://en.wikipedia.org/wiki/Dorsol...frontal_cortex

As the DLPFC undergoes long maturational changes, one change that has been attributed to the DLPFC for making early cognitive advances is the increasing level of the neurotransmitter dopamine in the DLPFC. In studies where adult macaques' dopamine receptors were blocked, it was seen that the adult macaques had deficits in the A-not-B task, as if the DLPFC was taken out altogether. A similar situation was seen when the macaques were injected with MPTP, which reduces the level of dopamine in the DLPFC. Even though there have been no physiological studies about involvement of cholinergic actions in sub-cortical areas, behavioral studies indicate that the neurotransmitter acetylcholine is essential for working memory function of the DLPFC.

[Petter]

https://i.imgur.com/V2oDfxq.jpg





https://klinglerlab.org/research/





https://en.wikipedia.org/wiki/Central_nucleus_of_the_amygdala

The central nucleus of the amygdala (CeA or aCeN) is a nucleus within the amygdala. It "serves as the major output nucleus of the amygdala and participates in receiving and processing pain information."





https://www.researchgate.net/figure/...o_fig1_5915826

Thus the medial part of the central amygdala may be involved in integrating information from external (e.g., food) and internal worlds (e.g., hunger/satiety). This integration allows for promoting adequate physiologicaland behavioral responses.

[...]

In aggregate, the most plausible explanation for the functional role of the medial part of the central amygdala seems to be that it serves to coordinate acquisition of alimentary/gustatory behaviors. On the other hand, the lateral subdivision appears to be mainly involved in attention and vigilance.





https://www.sciencedirect.com/topics/immunology-and-microbiology/medial-amygdala

The amygdala is comprised of at least three primary regions: basolateral complex of the amygdala (BLA), central amygdala (CeA), and medial amygdala. All these regions comprise distinct nuclei.

[...]

The medial amygdala (MA) is a complex amygdaloid structure that is both part of the “extended amygdala” and a key node in the social behavior network. It is superficial to basolateral and basomedial amygdala and lateral to the optic tract and is composed of several subnuclei with differing structure, development, and function. In many vertebrates, MA is strongly linked to defensive and social chemosensory function because of its extensive interconnections with main and accessory olfactory systems. MA also contains subnuclei that are highly steroid-sensitive and connect to other similarly sensitive structures, including the basal forebrain and hypothalamic nuclei regulating steroid-dependent social behaviors. Functionally, MA is consistently implicated in control of social and defensive/stress-related behaviors as well as the regulation of concomitant physiological responses. Thus, MA appears to integrate both internal state and external emotionally charged cues in order to coordinate adaptive responses within social and emotional contexts.

[...]

The amygdala is a collection of nuclei that contribute to learning, motivation, and fear (central nucleus and basolateral division) and chemosensory processing and social behaviors (corticomedial division). The medial amygdala is larger in males than in females, and the corticomedial region is critical for integration of chemosensory, genitosensory, and hormonal stimuli. Corticomedial lesions impair copulation, with the severity dependent on the specific location and species. The posterodorsal medial amygdala (MeApd) is one site at which serotonin 5-HT1A agonists facilitate copulation. A subregion of the MeApd is linked to sexual satiety.

[...]

The medial nucleus of the amygdala (MA) plays a critical role sorting chemosensory information to determine the sex and hormonal state of conspecifics. As the integrating hub of the social behavior and social decision-making networks, the MA regulates a variety of social behaviors, including mating. The structure and function of the MA are regulated by circulating gonadal hormones and influenced by social experience. Furthermore, each of the three major subdivisions of MA maintains differential connections that dictate specific roles in social behaviors.





https://pubmed.ncbi.nlm.nih.gov/26536109/

Here we show that the basomedial amygdala (BMA) represents the major target of ventral mPFC in amygdala in mice. Moreover, BMA neurons differentiate safe and aversive environments, and BMA activation decreases fear-related freezing and high-anxiety states. Lastly, we show that the ventral mPFC-BMA projection implements top-down control of anxiety state and learned freezing, both at baseline and in stress-induced anxiety, defining a broadly relevant new top-down behavioural regulation pathway.





https://www.sciencedirect.com/topics...teral-amygdala

The lateral amygdala (LA) is regarded as the sensory input gateway, receiving information from both the thalamus and the cortical areas, including polysensory areas and the prefrontal cortex (PFC).





https://www.sciencedirect.com/topics...tical-amygdala

Consistently, optogenetic inhibition of CoA reduces innate responses to the odors of both positive and negative valence (Root, Denny, Hen, & Axel, 2014). Interestingly, neurons activated by odors of positive or neutral valence are mainly recruited in the posterior section of the CoA, compared to neurons activated by an odor of negative valence which is equally distributed in the anteroposterior axis (Root et al., 2014).



------



https://www.sciencedirect.com/scienc...06322321000354

https://i.imgur.com/fHd894s.jpg

Figure 2. Circuit basis for amygdala regulation of the HPA axis activity. Amygdala subnuclei, including the BLA, CeA, and MeA, modulate the HPA axis activity primarily through some intermediate nuclei, including the BNST, NTS, DMH, and mPOA, which send efferent fibers to the PVN. ac, anterior commissure; ACTH, adrenocorticotropic hormone; alBNST, anterolateral BNST; avBNST, anteroventral BNST; BLA, basolateral amygdala; BNST, bed nucleus of the stria terminalis; CeA, central amygdala; CRF, corticotropin-releasing factor; dBNST, dorsal BNST; dmDMH, dorsomedial DMH; DMH, dorsomedial hypothalamus; GABAergic, gamma-aminobutyric acidergic; HPA, hypothalamic-pituitary-adrenal; LA, lateral amygdala; MeA, medial amygdala; mPOA, medial preoptic area; NTS, nucleus of the solitary tract; pBNST, posterior BNST; PVN, paraventricular nucleus of the hypothalamus; vlDMH, ventrolateral DMH.





https://www.frontiersin.org/journals...012.00033/full

Figure 9

PMV = premammillary nucleus, ventral part

MPO = medial preoptic nucleus





https://i.imgur.com/F4D62R9.png





https://i.imgur.com/EXVdkVb.jpg





https://i.imgur.com/CppTM3o.jpg

[Petter]

https://pubmed.ncbi.nlm.nih.gov/35863332/

Oxytocin and vasopressin are peptide hormones secreted from the pituitary that are well known for their peripheral endocrine effects on childbirth/nursing and blood pressure/urine concentration, respectively. However, both peptides are also released in the brain, where they modulate several aspects of social behaviors. Oxytocin promotes maternal nurturing and bonding, enhances social reward, and increases the salience of social stimuli. Vasopressin modulates social communication, social investigation, territorial behavior, and aggression, predominantly in males. Both peptides facilitate social memory and pair bonding behaviors in monogamous species.

[Petter]

human needs


1. physiological needs: air, water, food, warmth, sleep


2. pleasure: mainly food (high in sugar) and sex ... avoidance of disgust


3. avoidance of pain <--> aggression/anger and fear


4. control/orientation (achieve goals and get rewarded) <--> excitement and frustration


5. attachment (love and mutual care) <--> empathy and crying (mirror neurons and oxytocin)


6. dominance (social hierarchy: show off achievements) <--> pride and shame (esteem needs)


7. play <--> laughing


8. meaningfulness <--> happiness and sadness

[Petter]

https://pubmed.ncbi.nlm.nih.gov/34341967/

Optimism is a personality trait strongly associated with physical and psychological well-being, with correlates in nonhuman species. Optimistic individuals hold positive expectancies for their future, have better physical and psychological health, recover faster after heart disease and other ailments, and cope more effectively with stress and anxiety. We performed a systematic review of neuroimaging studies focusing on neural correlates of optimism. A search identified 14 papers eligible for inclusion. Two key brain areas were linked to optimism: the anterior cingulate cortex (ACC), involved in imagining the future and processing of self-referential information; and the inferior frontal gyrus (IFG), involved in response inhibition and processing relevant cues. ACC activity was positively correlated with trait optimism and with the probability estimations of future positive events. Behavioral measures of optimistic tendencies investigated through the belief update task correlated positively with IFG activity.

------

happiness

a. meaningfulness

b. optimism

c. the gap between our expectations and reality

[Petter]

meaningfulness <--> the overall value of life (ACC)

[Petter]

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6519696/

Contrary to the view that the pACC subserves the processing of happiness and sACC that of sadness (Vogt et al. 2003), we did not find any cytoarchitectonic subdivision of pACC to be significantly linked to positively valenced emotions. Our results should not be interpreted in the sense that the pACC region is not involved in the processing of happiness, since when we specifically queried the BrainMap database for tasks belonging to the behavioral domain “happiness”, we found a total of 124 studies. However, only 5 of them reported activations within p24ab, 2 involved p24c, and 10 found a activations within p32, and there was not a significant convergence of activations within pACC areas compared with those located in other brain regions. Our results are in accordance with several previously published meta-analytic studies using quantitative or traditional literature search strategies which also failed to allocate the processing of positively valenced emotions to a specific cingulate region, or even to the cingulate gyrus (e.g., Phan et al. 2002; Vytal and Hamann 2010; Torta and Cauda 2011; Kirby and Robinson 2017). Thus, although the pACC by all means participates in the processing of positively valenced emotions, it cannot be categorized as being a “central hub” (van den Heuvel and Sporns 2013) in the network processing happiness (Salzman and Fusi 2010).

------

happiness = a lack of sadness (?)

[Petter]

https://en.wikipedia.org/wiki/Habenula

Neurons in the lateral habenula are 'reward-negative' as they are activated by stimuli associated with unpleasant events, the absence of the reward or the presence of punishment especially when this is unpredictable.

[...]

There has also shown to be an association with aberrant LHb activity and depression.





https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5125215/

In addition to representing signals associated with negative outcome, evidence is emerging to support the involvement of the LHb in goal-directed behaviors and behavioral flexibility (Kawai et al., 2015; Baker et al., 2016). Studies in nonhuman primates suggest that the anterior cingulate cortex (ACC) and the LHb both signal the negative outcome of choice and subsequently the adjustment of choice behaviors, albeit in distinct ways (Kawai et al., 2015).





https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5987018/

The LHb regulates reward prediction and reward learning, in part, through its glutamate projections to the rostromedial tegmental nucleus (RMTg), a brain region that sends inhibitory input to dopamine neurons in the ventral tegmental area (VTA). During negative RPEs, LHb neurons are activated and send excitatory signals to RMTg inhibitory neurons which project to and inhibit dopamine neuron firing (Matsumoto and Hikosaka, 2007; Jhou et al., 2009; Kaufling et al., 2009; Lammel et al., 2012; Figure ​Figure1).1). The LHb’s control over midbrain dopamine neurons is significant because inhibition of dopamine neuron firing is causally associated with negative RPEs and extinction learning (Steinberg et al., 2013; Chang et al., 2016, 2017). Furthermore, LHb activity does not correlate only with negative valence, but also acts as a center for negative RPE (Ullsperger and von Cramon, 2003; Salas et al., 2010; Bromberg-Martin and Hikosaka, 2011), as LHb neurons respond to reward information that is unexpectedly cued, delivered, or denied (Bromberg-Martin and Hikosaka, 2011). Thus, it appears that the LHb receives and processes negative RPE information in much the same way that dopamine neurons process positive RPE signals.





https://www.pnas.org/doi/full/10.1073/pnas.1323586111

Organisms must learn adaptively about environmental cue–outcome associations to survive. Studies in nonhuman primates suggest that a small phylogenetically conserved brain structure, the habenula, encodes the values of cues previously paired with aversive outcomes. However, such a role for the habenula has never been demonstrated in humans. We establish that the habenula encodes associations with aversive outcomes in humans, specifically that it tracks the dynamically changing negative values of cues paired with painful electric shocks, consistent with a role in learning. Importantly, habenula responses predicted the extent to which individuals withdrew from or approached negative and positive cues, respectively. These results suggest that the habenula plays a central role in driving aversively motivated learning and behavior in humans.

[...]

This position as a hub between corticolimbic networks and midbrain monoaminergic nuclei provides a means through which positively or negatively valenced stimuli can modulate motor output, leading to the hypothesis that the habenula plays a critical role in motivated behavior (5).

[...]

Furthermore, we found that the habenula is functionally coupled with the striatum, including the medial wall of the caudate, which is strongly innervated by dopamine neurons (15) and has previously been implicated in fMRI studies of Pavlovian aversive learning (13).





https://www.cambridge.org/core/journ...1EF15EEDA5035A

The habenula, which in humans is a small nuclear complex within the epithalamus, plays an essential role in regulating the intensity of reward-seeking and adversity-avoiding behavior in all vertebrate ancestors by regulating the activity of ascending midbrain monoaminergic tracts.

https://i.imgur.com/fM4atEZ.jpg

Figure 5

sCg = subgenual cingulate gyrus

LHb = lateral habenula


------


https://i.imgur.com/LsGoZ0b.jpg

The habenula regulates both happiness and sadness (increased excitement: green ... decreased excitement: yellow).

[Petter]

(see post #457 and #458)



https://i.imgur.com/nJtz5Ou.png

https://i.imgur.com/XegbQeQ.png

https://i.imgur.com/1b7Ts5O.png

https://i.imgur.com/ET8QaCG.png

https://i.imgur.com/Q4XEaIx.png


------


https://i.imgur.com/AsLY2Cq.jpg

https://i.imgur.com/ZSjIrWT.jpg


------


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3665907/

Further, the ventral mPFC was selectively associated with reward related tasks, while the dorsal mPFC was selectively associated with perspective-taking and episodic memory retrieval. The ventral mPFC is therefore predominantly involved in bottom-up-driven, approach/avoidance-modulating, and evaluation-related processing, whereas the dorsal mPFC is predominantly involved in top–down-driven, probabilistic-scene-informed, and metacognition-related processing in social cognition.





https://www.nature.com/articles/s41598-019-41544-z

Humans can rely on diverse sources of information to evaluate others, including knowledge (e.g., occupation, likes and dislikes, education, etc.) and perceptual cues (e.g., attractiveness, race, etc.). Previous research has identified brain regions supporting person evaluations, but are evaluations based on perceptual cues versus person-knowledge processed differently? Moreover, are neural responses consistent when person-knowledge is available but unnecessary for the evaluation? This fMRI study examined how the use and availability of person-knowledge shapes the neural underpinnings of social evaluations. Participants evaluated well-known actors based on attractiveness or body of work (i.e., person-knowledge) and unknown models based on attractiveness only. Analyses focused on the VMPFC, following research implicating this region in positive evaluations based on person-knowledge. The VMPFC was sensitive to the (1) availability of person-knowledge, showing greater responses as ratings became more positive for actors (but not models) regardless of rating dimension and (2) use of available person-knowledge, showing greater activity as ratings for likability based on body of work became more positive for actors versus models rated on attractiveness. These findings indicate that although brain regions supporting person evaluation are sensitive to the availability to person-knowledge, they are even more responsive when judgments require the use of available person-knowledge.





https://www.cell.com/neuron/pdf/S089...22)00463-9.pdf

Next, we review evidence showing that vmPFC translates values into choices. We consider work on perigenual ACC (pgACC), showing a role in integrating costs and benefits to drive behavior, and conclude by discussing how dorsomedial PFC (dmPFC) organizes relationships in social contexts.


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https://dictionary.apa.org/arousal

1. a state of physiological activation or cortical responsiveness, associated with sensory stimulation and activation of fibers from the reticular activating system.

2. a state of excitement or energy expenditure linked to an emotion. Usually, arousal is closely related to a person’s appraisal of the significance of an event or to the physical intensity of a stimulus. Arousal can either facilitate or debilitate performance.


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https://en.wikipedia.org/wiki/Reward_system

Primary rewards are a class of rewarding stimuli which facilitate the survival of one's self and offspring, and they include homeostatic (e.g., palatable food) and reproductive (e.g., sexual contact and parental investment) rewards. Intrinsic rewards are unconditioned rewards that are attractive and motivate behavior because they are inherently pleasurable. Extrinsic rewards (e.g., money or seeing one's favorite sports team winning a game) are conditioned rewards that are attractive and motivate behavior but are not inherently pleasurable. Extrinsic rewards derive their motivational value as a result of a learned association (i.e., conditioning) with intrinsic rewards. Extrinsic rewards may also elicit pleasure (e.g., euphoria from winning a lot of money in a lottery) after being classically conditioned with intrinsic rewards.

[...]

The reward system contains pleasure centers or hedonic hotspots – i.e., brain structures that mediate pleasure or "liking" reactions from intrinsic rewards. As of October 2017, hedonic hotspots have been identified in subcompartments within the nucleus accumbens shell, ventral pallidum, parabrachial nucleus, orbitofrontal cortex (OFC), and insular cortex.

(not ACC)


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lOFC and mOFC calculate the subjective value of a reward (or a punishment).

pgACC evaluates the cost and benefits of initiating a course of action.

sgACC drives changes in physiological arousal/excitement (happiness or sadness) and is involved in conditioned learning.

adACC deals with conflict-monitoring.

[Petter]

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1463181/

Darwin (1872/1965) considered anger to be an adaption that evolved as part of the action patterns designed to overcome a blockage of a desired goal. Consistent with Darwin’s view, early work with children found facial expressions of anger to be associated with or accompanied by increased instrumental responding to goal blockage (Amsel, 1962; Amsel & Roussel, 1952). More recent work reviewed by Lemerise and Dodge (2000) also demonstrated that from early infancy, anger in response to goal blockage is associated with attempts to overcome the obstacle. In contrast, sadness often occurs in the absence of any attempt to overcome a blocked goal (Lewis & Goldberg, 1969; Watson, 1972; White, 1959). Sadness in children can be accompanied by a belief in the inefficacy or inadequacy of one’s efforts or ability to deal with the obstacle (Dweck, 1991, 1998; Seligman, 1975). Work by Dweck and colleagues (e.g., Burhans & Dweck, 1995; Smiley & Dweck, 1994) suggests that sadness following failure is associated with less optimal patterns of achievement motivation, perceived competence, and self-worth in children.





https://www.sciencedirect.com/scienc...008?via%3Dihub

Drawing from the functional theory of emotion, anger is proposed to serve adaptive functions such as motivating children to persist in overcoming difficulties to achieve their goals, whereas sadness helps children to shift attention away from goals that they determine cannot be attained.


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https://www.nature.com/articles/s41598-018-26317-4

By applying graph analysis methods on functional connectivity between 20 regions of interest in 22 participants we identified two main brain network modules, one dorsal and one ventral, and their hub areas: the left dorsolateral prefrontal cortex (dlPFC) and the left medial frontal pole (mFP). These hub areas did not modulate their mutual functional connectivity following sadness but they did so through an interposed area, the subgenual anterior cingulate cortex (sACC). Our results identify dlPFC and mFP as areas regulating interactions between emotional and cognitive networks, and suggest that their modulation by sadness experience is mediated by sACC.

[...]

We applied here graph-theoretic network analysis to identify functional changes in brain networks associated with states of sharp emotional and cognitive contrast. Based on functional activations in concatenated working memory and sadness induction tasks, we identified two distributed brain networks, one comprising dorsal regions putatively associated with cognitive operation (dlPFC, IPS, iFG, mSFG, PCG) and another one comprising ventral regions linked to sadness processing (mFP, sACC, mOFG, Amy, Hip), which could be further decomposed in cortical and subcortical partitions. The modularity of these brain networks increased following sadness induction, consistent with the hypothesis that a sadness state increases the competition between emotional and cognitive subnetworks. Two areas emerged from our analysis as task-related connector hubs in the dorsal and ventral brain subnetworks based on their modulation by the sadness induction protocol: the dlPFCl in the dorsal community and the mFPl in the ventral subnetwork. Our data did not support direct interactions between these two hubs but instead coordination via an interposed area, the sACC, as the mediator of sadness-induced modulations in network structure.





https://www.sciencedirect.com/scienc...49763418306146

The neuroscience of sadness: A multidisciplinary synthesis and collaborative review


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https://pubmed.ncbi.nlm.nih.gov/32309893/

The role of the subgenual anterior cingulate cortex in dorsomedial prefrontal-amygdala neural circuitry during positive-social emotion regulation

Positive-social emotions mediate one's cognitive performance, mood, well-being, and social bonds, and represent a critical variable within therapeutic settings. It has been shown that the upregulation of positive emotions in social situations is associated with increased top-down signals that stem from the prefrontal cortices (PFC) which modulate bottom-up emotional responses in the amygdala. However, it remains unclear if positive-social emotion upregulation of the amygdala occurs directly through the dorsomedial PFC (dmPFC) or indirectly linking the bilateral amygdala with the dmPFC via the subgenual anterior cingulate cortex (sgACC), an area which typically serves as a gatekeeper between cognitive and emotion networks. We performed functional MRI (fMRI) experiments with and without effortful positive-social emotion upregulation to demonstrate the functional architecture of a network involving the amygdala, the dmPFC, and the sgACC. We found that effortful positive-social emotion upregulation was associated with an increase in top-down connectivity from the dmPFC on the amygdala via both direct and indirect connections with the sgACC. Conversely, we found that emotion processes without effortful regulation increased network modulation by the sgACC and amygdala. We also found that more anxious individuals with a greater tendency to suppress emotions and intrusive thoughts, were likely to display decreased amygdala, dmPFC, and sgACC activity and stronger connectivity strength from the sgACC onto the left amygdala during effortful emotion upregulation. Analyzed brain network suggests a more general role of the sgACC in cognitive control and sheds light on neurobiological informed treatment interventions.





https://www.pnas.org/doi/full/10.1073/pnas.1317695111

The subgenual anterior cingulate cortex (subgenual ACC) plays an important role in regulating emotion, and degeneration in this area correlates with depressed mood and anhedonia. Despite this understanding, it remains unknown how this part of the prefrontal cortex causally contributes to emotion, especially positive emotions. Using Pavlovian conditioning procedures in macaque monkeys, we examined the contribution of the subgenual ACC to autonomic arousal associated with positive emotional events. After such conditioning, autonomic arousal increases in response to cues that predict rewards, and monkeys maintain this heightened state of arousal during an interval before reward delivery. Here we show that although monkeys with lesions of the subgenual ACC show the initial, cue-evoked arousal, they fail to sustain a high level of arousal until the anticipated reward is delivered. Control procedures showed that this impairment did not result from differences in autonomic responses to reward delivery alone, an inability to learn the association between cues and rewards, or to alterations in the light reflex. Our data indicate that the subgenual ACC may contribute to positive affect by sustaining arousal in anticipation of positive emotional events. A failure to maintain positive affect for expected pleasurable events could provide insight into the pathophysiology of psychological disorders in which negative emotions dominate a patient’s affective experience.

[Petter]

disappointment: a negative experience ---> a few negative thoughts ---> ACC devalues a specific activity ---> habenula temporarily reduces excitement

sadness: a negative experience ---> persistent negative thoughts ---> ACC devalues all activities ---> habenula reduces excitement

happiness: a positive experience ---> persistent positive thoughts ---> ACC upgrades the value of all activities ---> habenula raises excitement

[Petter]

https://www.medicalnewstoday.com/art...d-primal-fears

Over the years, since Darwin’s time, the similarities and differences between fear and disgust have been debated. It is now established that the physiological responses are different: fear activates the sympathetic nervous system, and disgust triggers the parasympathetic nervous system.

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Spoiled food does not attack people so there is no need to freeze or run away from it :-)

[Petter]

aggression/anger

1. avoid pain

2. defend resources ... this is probably correct

[Petter]

https://sites.dartmouth.edu/dujs/202...es-and-humans/

One day at the San Diego Zoo, an old male bonobo named Kakowet suddenly began screaming and frantically waving his arms at the zookeepers. After noticing Kakowet’s odd behavior, the keepers checked his surroundings to find several young bonobos stuck in a two-meter-deep moat filling up with water. The zookeepers rescued all but one ape, who was pulled out by Kakowet himself (de Waal, 1997). Kakowet’s behavior is certainly emotional and helpful, but is it enough to be called empathy?

In the past two decades, biologists have started to question whether empathy—the ability to understand another’s perspective and share their emotions—is uniquely human. The most basic level of empathy is emotional contagion, such as when human babies cry upon hearing the wails of other infants. This ability is present at birth for humans but also exists in young apes, who throw temper tantrums to make their mothers more distressed and thus pay more attention to them (Potegal, 2000). The second level of empathy is sympathetic concern, which appears around two years old in humans when toddlers try to console someone in distress. Apes also readily display this quality, such as when they wrap an arm around another member who lost in a fight (de Waal & van Roosmalen, 1979). Kakowet above has demonstrated emotional contagion by sharing the distress of the young bonobos stuck in a moat, as well as sympathetic concern in his attempt to help them.

However, scientists disagree on whether great apes possess the most advanced layer of empathy, empathic perspective-taking, which develops in humans after four years old. It first requires understanding that one’s own needs can be different from someone else’s, then thinking from that other person’s perspective, all while being emotionally involved. One empathy model by primatologist Frans de Waal (2008) proposes that great apes have all three levels of empathy. On the other hand, another model by biologists Sonja Koski and Elisabeth Sterck (2010) posits that apes do not have empathic perspective-taking, only reaching the equivalent of a human two-year-old’s empathy.

According to the first model, great apes can form a mental understanding of the specific situation where a member is in need, then adapt their behavior accordingly (de Waal, 2008). In doing so, they display the ability to distinguish their own view from someone else’s, as well as the ability to think from the other’s perspective. For example, Kakowet must have put himself in the young apes’ viewpoint to realize that they were too small to escape from the moat. He then acted distressed toward the zookeepers because he understood that they were the best ones to call for help. This targeted helping demonstrates Kakowet’s empathic perspective-taking as a chimpanzee.

However, Koski and Sterck’s model outlines that great apes’ helping behavior cannot prove the existence of full perspective-taking. Specifically, they may confuse another ape’s mental state with their own: even though Kakowet himself is not in any danger, he becomes frantic like the young bonobos. Koski and Sterck would say he is simply exhibiting emotional contagion, which is only the first level of empathy. In a similar situation, most human adults would act calmer than Kakowet. Other behaviors in apes, such as tending to another’s wounds or reconciling after a conflict, also do not necessarily require perspective-taking. In this sense, apes have not reached a level of empathy comparable to a human adult (Koski and Sterck, 2010). By diving deeper into the mental states of great apes, Koski and Sterck effectively modify de Waal’s old model.

What do these findings reveal about how empathy evolved? Given that humans and great apes share the first two levels of empathy, it is likely that their last common ancestor already had considerable abilities to socialize with others. Despite not being able to engage in full perspective-taking, their sympathetic concern—in combination with emotional contagion—would have helped them reproduce and thrive. For humans, perspective-taking in empathy likely evolved alongside the intricate social rules and hierarchies (Radzvilavicius et al., 2019). In addition, the development of language may have boosted the uniquely human ability for complex reasoning and empathic perspective-taking (Hodges et al., 2018).

Due to the lack of consensus on the experimental paradigms with high internal validity, little to no studies have directly investigated how great apes mentally process their acts of empathy (Koski and Sterck, 2010). Does empathic perspective-taking depend on a specific region exclusive to humans? Can the differences between human and ape empathy be traced back to anatomical variations in the brain? Future research could utilize brain scanning techniques to investigate the neural underpinnings of empathy.

[Petter]

reasons for violence

1. money (resources)

2. low self-esteem (indirectly related to resources)

3. injustice

4. a health emergency

5. mental illness

6. learned behavior from growing up in a family where domestic violence was accepted

7. alcohol and drugs

8. cultural beliefs that a man has the right to control his wife (a resource)

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4-7 are irrelevant here

[Petter]

https://www.verywellmind.com/overcom...rriage-2303979

love and mutual care ---> infidelity ---> betrayal (injustice) ---> violence

Why? Because he/she had a misguided sense of ownership over the partner (a resource).

[Petter]

https://en.wikipedia.org/wiki/Bullying

1. A person wants someone to leave a territory (a resource).

2. "Individual bullying is usually characterized by a person behaving in a certain way to gain power over another person."

"Robert W. Fuller has analyzed bullying in the context of rankism." (esteem needs are indirectly related to resources)