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Thread: Basic Emotions

  1. #401
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    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6043598/

    In fact, the emotion of anger, which is defined as a negative emotional response to goal-blockage and unfair behavior by others, is conceptually distinct from aggression, which is defined as an action intended to cause harm to another individual.
    An emotional response to a destruction of an obstacle is perhaps a better definition of anger.

    (recklessness)

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    https://europepmc.org/article/med/33748351

    The positive affect of rewards is an important contributor to well-being. Reward involves components of pleasure 'liking', motivation 'wanting', and learning. 'Liking' refers to the hedonic impact of positive events, with underlying mechanisms that include hedonic hotspots in limbic brain structures that amplify 'liking' reactions. 'Wanting' refers to incentive salience, a motivational process that makes reward cues attractive and able to trigger craving for their reward, mediated by larger dopamine-related mesocorticolimbic networks. Under normal conditions, 'liking' and 'wanting' cohere. However, 'liking' and 'wanting' can be dissociated by alterations in neural signaling, either induced in animal neuroscience laboratories or arising spontaneously in addictions and other affective disorders, which can be detrimental to positive well-being.

    wanting and liking.jpg

    wanting and liking 2.jpg

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    https://pubmed.ncbi.nlm.nih.gov/26547313/

    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.

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    euphoria (i.e. intense feelings of well-being) <--> hedonic hotspots ('liking')

    euphoria ---> meaningfulness ---> positive mood (happiness) ... epithalamus

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

    Cognitive appraisal: provides an evaluation of events and objects.

    Bodily symptoms: the physiological component of emotional experience.

    * Action tendencies: a motivational component for the preparation and direction of motor responses.

    Expression: facial and vocal expression almost always accompanies an emotional state to communicate reaction and intention of actions.

    Feelings: the subjective experience of emotional state once it has occurred.

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

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    https://www.scientificamerican.com/a...t-found-brain/

    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.

    [...]

    With the help of powerful neuroimaging techniques, we have found that the activity of a small region within the orbitofrontal cortex, called the midanterior site, correlates tightly with the subjective pleasantness of a nice sensation, such as the taste of chocolate milk. At the first sip, for example, the site is alight with activity. Yet once subjects have consumed enough of the sweet stuff, the midanterior site shuts down, rendering the experience no longer pleasurable.

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    1.
    euphoria ---> meaningfulness ---> positive mood (happiness) ... epithalamus

    2. pleasure (or a lack of pain) ---> meaningfulness ---> euphoria (feeling energized or 'high') ---> positive mood

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    blue: excitement

    grey: attention/interest ... this could be a basic emotion

    green: fear

    red: anger

    ------

    hypothalamus functions 12.jpg

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    http://www.tomkins.org/what-tomkins-...d-personality/

    Interest-Excitement: The pull toward mastery

    Inherently rewarding

    An intensity of gaze, eyebrows down, “track, look, listen” is the face of interest. High intensity excitement usually involves muscle movement and vocalization. The purpose of interest is to make learning rewarding. Interest is the most seriously neglected of the affects, possibly because it doesn’t disrupt thinking, but often fuels it. And since emotions are so often seen to be at odds with rational thought, it has escaped the attention of devoted thinkers that there is a good feeling associated with thinking. That good feeling is interest. “The interrelationships between the affect of interest and the functions of thought and memory are so extensive that the absence of the affective support of interest would jeopardize intellectual development no less than destruction of brain tissue. To think, as to engage in any other human activity, one must care, one must be excited, must be continually rewarded.” (Affect Imagery Consciousness, Vol. I p. 343) Interest is triggered by a gradual, manageable increase in neural firing. We can see it on infants’ faces as they encounter new sights, sounds and sensations.

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    excitement <--> a reward

    interest <--> learning (a reward?)
    Last edited by Petter; 10-13-2023 at 08:41 AM.

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    anger <--> destroy an obstacle

    interest <--> outsmart an obstacle

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    https://www.intechopen.com/chapters/53113

    Within the medial PFC, the orbitofrontal cortex (OFC) plays a particularly noteworthy role, because it is essential for regulating the direction of motivation.

    [...]

    The habenula constitutes—together with the stria medullaris and pineal gland—the epithalamus and consists of medial and lateral parts. The habenula regulates the intensity of reward-seeking and misery-fleeing behaviour probably in all our vertebrate ancestors.

    habenula and mPFC.png

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    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8363507/

    The anterior thalamic nuclei are a vital node within hippocampal-diencephalic-cingulate circuits that support spatial learning and memory. Reflecting this interconnectivity, the overwhelming focus of research into the cognitive functions of the anterior thalamic nuclei has been spatial processing. However, there is increasing evidence that the functions of the anterior thalamic nuclei extend beyond the spatial realm. This work has highlighted how these nuclei are required for certain classes of temporal discrimination as well as their importance for processing other contextual information; revealing parallels with the non-spatial functions of the hippocampal formation. Yet further work has shown how the anterior thalamic nuclei may be important for other forms of non-spatial learning, including a critical role for these nuclei in attentional mechanisms. This evidence signals the need to reconsider the functions of the anterior thalamic within the framework of their wider connections with sites including the anterior cingulate cortex that subserve non-spatial functions.

    hypothalamus mammillary bodies.jpg

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    https://www.frontiersin.org/articles...017.00050/full

    Lateral Hypothalamic Control of the Ventral Tegmental Area: Reward Evaluation and the Driving of Motivated Behavior

    The LH → VTA circuit clearly plays an important role in driving behavior. Initial studies showed the importance of the LH in motivating basic functions such as mating, feeding, drinking, nest-building and gnawing, and the evidence that lesioning the LH results in a loss of these behaviors such as dramatic weight-loss, has highlighted the importance of this circuit for survival. Understanding this circuit will be important for understanding how normal behavior is elicited, and what is going wrong when these behaviors become disordered in cases such as obesity, anorexia, drug-abuse, anhedonia, etc. Considering the two main facets of goal-oriented behavior are the energizing and directing of behavior and what is known of the LH and VTA, it would appear that the LH neurons may play more of a role in the “driving” motivated behavior whereas the VTA likely directs the behavior toward relevant goals/rewards via the dopaminergic system for example, by modulating the reward-value of different environmental rewards. Although there are still many outstanding questions regarding the LH → VTA circuit, the development of new research technologies are allowing researchers more promising opportunities to probe this circuit and gain a more specific understanding of the basis for the dysregulation of this circuit and the negative behavioral consequences associated with it, such as drug abuse and obesity.

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    The activities of the NAcbC and NAcbS, in turn, are regulated by monoaminergic nuclei within the midbrain. These nuclei transmit signals through dopaminergic (ventral tegmental area), adrenergic (norepinephrine, locus coeruleus) and serotonergic (raphe nuclei) tracts. In addition to their direct regulation of the NAcbC and/or NAcbS, these monoaminergic nuclei regulate the activity of other, first relay station, basal ganglia and important parts of other areas in the forebrain. Therefore, it may be concluded that behavioural output is controlled at three levels within the brain. The highest level is the cerebral cortex (isocortex, limbic cortex, corticoid (cortical, basolateral) amygdala and hippocampal complex). The second level is the subcortical forebrain (dorsal striatum, ventral striatum, extended amygdala). The third level of control is the midbrain (monoaminergic regulation centres).

    As part of our model, we suggest that a fourth regulatory system exists, the habenula, which connects the cerebral cortex and midbrain systems (Figure 8).




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

    Evolution of circuits regulating pleasure and happiness with the habenula in control

    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.

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    midbrain and locus coeruleus.png

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    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

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    excitement ----- disappointment

    interest ----- boredom

    fear ----- relief

    anger ----- calmness, patience or thankfulness

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    I think awe, guilt, remorse, jealousy and other social emotions are variations of pride and shame.

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    https://www.sciencedirect.com/topics...social-emotion

    The Role of the MPFC in Self-Awareness

    Social emotions require that people be aware of the effects of their behavior on others, which necessitates self-awareness. That is, when people commit a faux pas, they must be able to recognize that the behavior they performed is inappropriate and that the feelings they are experiencing are embarrassment at having committed the faux pas. Self-awareness occurs when people themselves are the objects of their attention, such as when they think about themselves or process other information in a personal manner. Many years of research in psychology has revealed that information processed with reference to self seems to be treated “specially.”

    Converging evidence from patient research indicates that frontal lobe lesions, particularly to the MPFC and adjacent structures, have a deleterious effect on personality, mood, motivation, and self-awareness. Patients with frontal lobe lesions show dramatic deficits in recognizing their own limbs, engaging in self-reflection and introspection, identifying a faux pas as being socially inappropriate, and even reflecting on personal knowledge.

    A series of functional magnetic resonance imaging (fMRI) studies have also indicated that the MPFC plays a vital role in self-awareness. This region is more active, for example, when people report on their personality traits, make self-relevant judgments about pictures, or retrieve autobiographical memories of past events. Interestingly, the MPFC has also been identified as part of a “default network.” This network is active when the brain is at rest (ie, not engaged in an overt cognitive task). An abundance of neuroimaging data suggest that the default network plays a dominant role in self-awareness. As such, the default network supports important components of social emotions. The convergence of patient and imaging data support the conclusion that MPFC plays a prominent role in self-awareness, a necessary and critical contributor to the experience of social emotions.

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    Quora: "Envy is a byproduct of pride. Envy is the imaginary sense of shame that provokes a longing for objects of pride."

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    awe: Wow, that's very impressive! You should be proud of yourself.

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    https://en.wikipedia.org/wiki/Guilt_(emotion)

    "Guilt and shame are two closely related concepts, but they have key differences that should not be overlooked. Cultural Anthropologist Ruth Benedict describes shame as the result of a violation of cultural or social values, while guilt is conjured up internally when one's personal morals are violated. To put it more simply, the primary difference between shame and guilt is the source that creates the emotion. Shame arises from a real or imagined negative perception coming from others and guilt arises from a negative perception of one's own thoughts or actions."

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    guilt + empathy ---> anger, fear, sadness or shame

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    https://www.researchgate.net/publica...ilt_an_Emotion

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6960572/

    "... guilt is not an emotion, but a mere cognitive assessment of causing harm."

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    remorse = guilt + regret + self-directed resentment (anger)

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    https://www.sciencedirect.com/topics...l-hypothalamus (The lateral hypothalamus is a key brain structure linking changes in peripheral physiology to arousal.)

    Motivation Systems

    Primary efferents from the mPOA traveling through the lateral hypothalamus allow it to interact with components of the mesolimbic dopamine (DA) system for the motivational aspects of maternal responsiveness to pups. The mesolimbic DA system, which is composed of DA cell bodies in the midbrain VTA that project to the nucleus accumbens (NA) in the forebrain, has been recognized for its central role in several behavioral functions related to motivation. The NA receives converging excitatory inputs from most cortical and limbic structures, and hence has long been considered an interface linking those corticolimbic structures to behavioral output systems, under the modulatory influence of DAergic inputs from the VTA. Neurophysiological and neuroanatomical studies suggest that DA in the NA may select and integrate the effects of limbic and cortical afferents, thus influencing the transmission of information to output areas, and ultimately modulating goal-directed behaviors.

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    Glutamatergic and GABAergic neuronal populations

    Glutamatergic neurons of the lateral hypothalamus (LH) can increase their activity during escape behavior, including jumps, fear-like responses, and running away from a virtual attacker. Optogenetic inhibition (2-s pulse duration) of PAG-projecting glutamatergic (VGluT2) LH neurons precludes the capacity of mice to evaluate danger, whereas photostimulation at 20 Hz for 30 s of glutamatergic LH or PAG-projecting glutamatergic LH neurons induces evasion behavior. In contrast, GABAergic (VGAT) LH neurons increase their activity during predatory behavior; their photoinhibition (2-s pulse duration) blocks predatory attacks, whereas photostimulation at 20 Hz for 30 s of GABAergic LH-neurons or terminals in the PAG promotes a predatory behavior with initiation, chasing, and retrieval of a living or artificial prey. Interestingly, activation of PAG-projecting LH neurons without cell-type specificity produces predatory attacks as well, arguing that the GABAergic LH-PAG pathway for predation would overrule the glutamatergic LH-PAG pathway for evasion. Furthermore, in a real-time place preference test, activation of GABAergic LH terminals in the PAG induces avoidance behavior, whereas their inhibition induces approach behavior. This highlights the context dependency of these behavioral responses upon optogenetic manipulations of these neuronal populations.

    Steroidogenic factor 1 (SF1, presumably glutamatergic) neurons of the dorsomedial and central parts of the ventral medial hypothalamus VMH (dmcVMH) can generate a typical defensive-like response, including immobility and avoidance. Photostimulation of the dmcVMH induces immobility at low frequency (5–10 Hz) or low-power stimulation, while higher (15–20 Hz) frequency or higher power stimulation generates running and jumping. Furthermore, whereas activation of dmcVMH terminals to the dorsolateral PAG (dlPAG) induces immobility, activation of the anterior hypothalamus (AH) or dmcVMH terminals in the AH promotes escape behavior with jump and run. Interestingly, AH neurons are mainly GABAergic and project back to SF1-expressing dmcVMH neurons and to the PAG, thus suggesting that converging excitatory SF1 dmcVMH and inhibitory AH inputs might finetune the activity of the PAG to adapt over time the behavioral response to environmental threats.

    Similar to the AH, the zona incerta (ZI) contains a large population of GABAergic neurons, especially in its rostral part. Optogenetic activation at 20 Hz of GABAergic (GAD2) neurons of the rostral ZI or their axonal terminals to the PAG decreases running and distance traveled in response to a sound-induced flight reaction, whereas their photoinhibition increases this innate defensive behavior. Similarly, optogenetic activation of GABAergic ZI neurons or their axonal terminals to the PAG also reduces the percentage of freezing time in a conditioned freezing response pairing a sound and an electrical foot shock, whereas their photoinhibition increases this learned defensive behavior. Given that GABAergic neurons of the rostral ZI contact monosynaptically excitatory glutamatergic (VGluT2) neurons of the PAG, and the dorsolateral and ventrolateral part of the PAG trigger flight reaction and freezing, respectively, it is tempting to hypothesize that distinct GABAergic ZI neurons might modulate distinct PAG-triggered defensive behaviors.

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    Unique receptors expressed in layer 6b that can regulate state control

    Lateral hypothalamus will be discussed in Tamás’ chapter in detail. In lateral hypothalamus, there are neurons that produce a wake-promoting peptide, orexin. This peptide is essential for the stability of our arousal, lacking this peptide or its receptor can lead to sudden loss of arousal and sudden falling asleep. Neurons expressing the neuropeptides orexin-A and orexin-B are exclusively localized to the lateral hypothalamus and perifornical area (10,000–20,000 orexinergic neurons in the human brain) but they have wide projection targets across the central nervous system, including hypothalamus, thalamus, cortex, brain stem, and spinal cord. The projections to other hypothalamic neurons and subcortical arousal centers are important for modulating arousal, appetite, and activity of the hypothalamic–pituitary–adrenal axis. However, the roles of cortical projections remain less well understood.

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    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6372319/

    A time to fight: circadian control of aggression and associated autonomic support

    The central circadian clock, located in the suprachiasmatic nucleus of the mammalian hypothalamus (SCN), regulates daily behavioral rhythms including the temporal propensity for aggressive behavior. Such aggression propensity rhythms are regulated by a functional circuit from the SCN to neurons that drive attack behavior in the ventromedial hypothalamus (VMH), via a relay in the subparaventricular zone (SPZ). In addition to this pathway, the SCN also regulates sleep-wake and locomotor activity rhythms, via the SPZ, in a circuit to the dorsomedial hypothalamus (DMH), a structure that is also known to play a key role in autonomic function and the sympathetic “fight-or-flight” response (which prepares the body for action in stressful situations such as an agonistic encounter). While the autonomic nervous system is known to be under pronounced circadian control, it is less apparent how such autonomic rhythms and their underlying circuitry may support the temporal propensity for aggressive behavior. Additionally, it is unclear how circadian and autonomic dysfunction may contribute to aberrant social and emotional behavior, such as agitation and aggression. Here we review the literature concerning interactions between the circadian and autonomic systems and aggression, and we discuss the implications of these relationships for human neural and behavioral pathologies.

    [...]

    The DMH also projects to orexin neurons in the lateral hypothalamus (LH), which have been suggested to regulate the hyperarousal during fight-or-flight responses.

    [...]

    As further evidence of the interconnectedness of these systems, sympathethic preganglionic fibers project to the adrenal medulla and stimulate the release of catecholamines into the bloodstream to support bodily action during the fight-or-flight response (Kvetnansky et al., 1995). Indeed, lower than normal levels of catecholamine activity have been shown to be associated with greater levels of anger and agitation in adult humans (Schwartz and Portnoy, 2017).

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    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5787107/

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    https://www.frontiersin.org/articles...017.00094/full

    Aggression is a costly behavior, sometimes with severe consequences including death. Yet aggression is prevalent across animal species ranging from insects to humans, demonstrating its essential role in the survival of individuals and groups. The question of how the brain decides when to generate this costly behavior has intrigued neuroscientists for over a century and has led to the identification of relevant neural substrates. Various lesion and electric stimulation experiments have revealed that the hypothalamus, an ancient structure situated deep in the brain, is essential for expressing aggressive behaviors. More recently, studies using precise circuit manipulation tools have identified a small subnucleus in the medial hypothalamus, the ventrolateral part of the ventromedial hypothalamus (VMHvl), as a key structure for driving both aggression and aggression-seeking behaviors. Here, we provide an updated summary of the evidence that supports a role of the VMHvl in aggressive behaviors. We will consider our recent findings detailing the physiological response properties of populations of VMHvl cells during aggressive behaviors and provide new understanding regarding the role of the VMHvl embedded within the larger whole-brain circuit for social sensation and action.

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    https://en.wikipedia.org/wiki/Frustr...ion_hypothesis

    When first formulated, the hypothesis stated that frustration always precedes aggression, and aggression is the sure consequence of frustration. Two years later, however, Miller and Sears re-formulated the hypothesis to suggest that while frustration creates a need to respond, some form of aggression is one possible outcome. Therefore, the re-formulated hypothesis stated that while frustration prompts a behavior that may or may not be aggressive, any aggressive behavior is the result of frustration, making frustration not sufficient, but a necessary condition for aggression.

    [...]

    The publication of Frustration and Aggression gave rise to criticism from several scientists, including animal behaviorists, psychologists, and psychiatrists. For example, Seward, who studied rat behavior, suggested that aggression can also be caused by dominance struggles, which for him were different from frustration. Durbin and Bowlby, by observing apes and children, placed reasons for the breaking out of a fight into three different categories. While one of the categories was frustration, the other two were classified as possession disputes and resentment of a stranger intrusion. Addressing this criticism, Berkowitz suggested that the controversy around the frustration-aggression hypothesis has its roots in the lack of a common definition for frustration. He advocated that if frustration is defined as a reaction to a blocking of a drive or an interruption of some internal response sequence, those various reasons for aggression actually fall under the frustration umbrella.

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    https://onlinelibrary.wiley.com/doi/....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.

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    https://www.sciencedirect.com/scienc...91305715300903

    Frustration can be defined as an emotional state generated by the omission or devaluation in the quantity or quality of an expected appetitive reward. Thus, reactivity to a reward is affected by prior experience with the different reinforcer values of that reward. This phenomenon is known as incentive relativity, and can be studied by different paradigms. Although methodologically simple, the exploration of a novel open field (OF) is a complex situation that involves several behavioral processes, including stress induction and novelty detection. OF exposure can enhance or block the acquisition of associative and non-associative memories. These experiments evaluated the effect of OF exploration on frustration and the role played by the cholinergic system in this phenomenon. OF exploration before first or second trial of incentive downshift modulated the expression of frustration. This effect of OF was blocked by the administration of scopolamine either before or after OF exploration. These results indicate that the cholinergic system is involved in the acquisition and consolidation of OF information.

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

    The mammillary bodies do not have interneurons. The processing of information within the mammillary bodies occurs from projection neurons of other regions of the brain. It receives both dopaminergic and acetylcholine reciprocal projections from the tegmentum (blue line, Figure 1C) that help to regulate what information the mammillary bodies send forward to the anterior thalamic nucleus (Papez circuit) and the cerebellum. Because tegmental connections are reciprocal (bi-directional), the mammillary activity also influences the tegmentum and other connections of the tegmentum (e.g., amygdala, prefrontal cortex, hippocampus, and nucleus accumbens). Activation of the acetylcholine and dopamine circuits activate norepinephrine and serotonin systems downstream. Each of these neurotransmitter systems helps to mediate memory storage within the cortex. They also help to facilitate other limbic functions (e.g., attention, learning, memory, motor systems, decision, planning, and emotion).

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    https://www.kenhub.com/en/library/anatomy/hypothalamus

    The mammillary region is the most posterior of the four medial zone regions. This region lies internal to the mammillary bodies and contains the medial, intermediate, and lateral mammillary nuclei, which collectively form the mammillary complex, the tuberomammillary nucleus and the posterior hypothalamic nucleus. The large medial mammillary nucleus is the main point of termination for axons of the postcommissural fornix, which arise from the hippocampal complex and relays input related to emotions. This nucleus also connects to the anterior nucleus of the dorsal thalamus via the mammillothalamic tract and forms an important part of the limbic system. The smaller intermediate and lateral mammillary nuclei have connections to the midbrain reticular formation. The mammillary nuclei play a role in the processing of immediate memory or short-term memory. The tuberomammillary nucleus contains histaminergic neurons and is involved in the promotion of wakefulness. The posterior hypothalamic nucleus is closely related to the midbrain periaqueductal gray and as such plays a similar role as this midbrain region in the modulation of emotion, cardiovascular function and pain modulation. The posterior hypothalamic nucleus also acts as a “thermostat” regulating body temperature.

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    https://www.researchgate.net/figure/...e_fig3_5235838

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    https://www.medrxiv.org/content/10.1...1257119v1.full

    In the past decades, researchers have attempted to model the core neural features of reactive aggression. For instance, it has been argued that the medial hypothalamus, amygdala and the PAG are crucial nodes for understanding retaliatory behaviors (Bertsch et al., 2020; Blair, 2016; Crowe & Blair, 2008; Gregg & Siegel, 2001; Lickley & Sebastian, 2018; Panksepp, 2004; Panksepp & Zellner, 2004).

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    https://journals.sagepub.com/doi/ful...33102412443336

    From a pathophysiological perspective, there is good evidence for the involvement of the ventro- and dorsomedial as well as the posterior hypothalamus in the pathophysiology of aggression. Interventional data from animal experiments and stereotactic neurosurgery of the posterior hypothalamic region in humans have shown striking effects on aggressive behaviour. However, aggression cannot be reduced to the hypothalamic system alone. Extensive changes in neurotransmitter release have been described in an intricate network of areas such as the orbitofrontal and the anterior cingulate cortex (top-down control) and limbic structures, mainly the amygdala.
    Last edited by Petter; 12-05-2023 at 02:16 PM.

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    posterior hypothalamus <--> frustration

    ventromedial and dorsomedial hypothalamus <--> aggression

    (?)

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    https://www.frontiersin.org/articles...012.00589/full

    Affective neuronal selection: the nature of the primordial emotion systems ... Judith A. Toronchuk and George F. R. Ellis

    Based on studies in affective neuroscience and evolutionary psychiatry, a tentative new proposal is made here as to the nature and identification of primordial emotional systems. Our model stresses phylogenetic origins of emotional systems, which we believe is necessary for a full understanding of the functions of emotions and additionally suggests that emotional organizing systems play a role in sculpting the brain during ontogeny. Nascent emotional systems thus affect cognitive development. A second proposal concerns two additions to the affective systems identified by Panksepp. We suggest there is substantial evidence for a primary emotional organizing program dealing with power, rank, dominance, and subordination which instantiates competitive and territorial behavior and is an evolutionary contributor to self-esteem in humans. A program underlying disgust reactions which originally functioned in ancient vertebrates to protect against infection and toxins is also suggested.

    basic emotions Toronchuk and Ellis.png

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    blue interacts with grey, green and red (excitement)

    grey: learning (attention/interest)

    green: parental care and social bonding

    red: survival and reproduction ... feed-and-breed <--> fight-or-flight (anger and fear)

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    hypothalamus functions 12.jpg

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    https://www.jneurosci.org/content/40/48/9283

    Differential Encoding of Predator Fear in the Ventromedial Hypothalamus and Periaqueductal Grey

    The ventromedial hypothalamus is a central node of the mammalian predator defense network. Stimulation of this structure in rodents and primates elicits abrupt defensive responses, including flight, freezing, sympathetic activation, and panic, while inhibition reduces defensive responses to predators. The major efferent target of the ventromedial hypothalamus is the dorsal periaqueductal gray (dPAG), and stimulation of this structure also elicits flight, freezing, and sympathetic activation. However, reversible inhibition experiments suggest that the ventromedial hypothalamus and periaqueductal gray play distinct roles in the control of defensive behavior, with the former proposed to encode an internal state necessary for the motivation of defensive responses, while the latter serves as a motor pattern initiator. Here, we used electrophysiological recordings of single units in behaving male mice exposed to a rat to investigate the encoding of predator fear in the dorsomedial division of the ventromedial hypothalamus (VMHdm) and the dPAG. Distinct correlates of threat intensity and motor responses were found in both structures, suggesting a distributed encoding of sensory and motor features in the medial hypothalamic-brainstem instinctive network.

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    https://www.nature.com/articles/npp200855

    These findings suggest that multiple outputs from the amygdala play a critical role in fear-potentiated startle and that SP (substance P) plays a critical, probably modulatory role, in the MeA to VMH to PAG to the startle pathway based on these and data from others.
    Last edited by Petter; 12-07-2023 at 08:57 AM.

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    https://resultscoachingglobal.com/cu...hem-different/

    "Interest is a cognitive openness to engaging with a topic or experience.

    Curiosity is recognizing a gap in our knowledge about something that interests us and becoming emotionally and cognitively invested in closing that gap through exploration and learning. Curiosity often starts with interest and can range from mild curiosity to passionate investigation."

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    ventromedial and dorsomedial hypothalamus: frustration ---> anger ---> aggression

    VMH, DMH and posterior hypothalamus: rage ... the sympathetic nervous system is activated

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    https://pubmed.ncbi.nlm.nih.gov/25229197/

    Disgust is a prototypical type of negative affect. In animal models of excessive disgust, only a few brain sites are known in which localized dysfunction (lesions or neural inactivations) can induce intense 'disgust reactions' (e.g. gapes) to a normally pleasant sensation such as sweetness. Here, we aimed to map forebrain candidates more precisely, to identify where either local neuronal damage (excitotoxin lesions) or local pharmacological inactivation (muscimol/baclofen microinjections) caused rats to show excessive sensory disgust reactions to sucrose. Our study compared subregions of the nucleus accumbens shell, ventral pallidum, lateral hypothalamus, and adjacent extended amygdala. The results indicated that the posterior half of the ventral pallidum was the only forebrain site where intense sensory disgust gapes in response to sucrose were induced by both lesions and temporary inactivations (this site was previously identified as a hedonic hotspot for enhancements of sweetness 'liking'). By comparison, for the nucleus accumbens, temporary GABA inactivations in the caudal half of the medial shell also generated sensory disgust, but lesions never did at any site. Furthermore, even inactivations failed to induce disgust in the rostral half of the accumbens shell (which also contains a hedonic hotspot). In other structures, neither lesions nor inactivations induced disgust as long as the posterior ventral pallidum remained spared. We conclude that the posterior ventral pallidum is an especially crucial hotspot for producing excessive sensory disgust by local pharmacological/lesion dysfunction. By comparison, the nucleus accumbens appears to segregate sites for pharmacological disgust induction and hedonic enhancement into separate posterior and rostral halves of the medial shell.
    lateral hypothalamus <--> 'wanting'

    hedonic coldspot <--> disgust, 'disliking' (---> dysphoria)

    Disgust is not a basic emotion.

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    MESOCORTICOLIMBIC-HYPOTHALAMIC CIRCUITRY AND FUNCTIONS.jpg

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

    Action tendencies: a motivational component for the preparation and direction of motor responses.
    lateral hypothalamus <--> nucleus accumbens and ventral pallidum (pleasure)

    ventromedial and dorsomedial hypothalamus <--> PAG (pain)

    the mammillary bodies <--> anterior thalamic nuclei and hippocampus (attention/interest, learning, memory)

    Interest does not deal with motivation so it is not a basic emotion.
    Last edited by Petter; 12-09-2023 at 09:49 AM.

  35. #435
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    3 basic emotions

    excitement

    anger

    fear

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    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8884703/

    The startle reflex in humans is a conserved systemic motion response that is ubiquitous in mammals. It is the reflex contraction of the skeletal and facial muscles to sudden intense stimuli, and includes eye blinking, limb flexion, trunk shrugs, and autonomic symptoms (such as increased heart rate, sweating).

    [...]

    The main pathway of the startle reflex is the reticulospinal tract, beginning from the medulla oblongata and pons, and running parallel to the corticospinal tract that innervates skeletal muscle movement.


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    https://www.jneurosci.org/content/41/11/2447

    Surprise: Unexpected Action Execution and Unexpected Inhibition Recruit the Same Fronto-Basal-Ganglia Network

    Unexpected and thus surprising events are omnipresent and oftentimes require adaptive behavior such as unexpected inhibition or unexpected action. The current theory of unexpected events suggests that such unexpected events just like global stopping recruit a fronto-basal-ganglia network. A global suppressive effect impacting ongoing motor responses and cognition is specifically attributed to the subthalamic nucleus (STN).

    [...]

    Unexpected events are omnipresent and usually require rapid adaptation of ongoing behavior. For example, a car driver must brake when a kid runs onto the road. Such situations require reactive control when unexpected stimuli signal the need to rapidly cancel ongoing actions and to initiate new, situationally more appropriate behaviors. Reactive control is thus necessary to avoid harmful consequences, making it essential for adaptive behavior.

    The neural underpinnings of reactive motor control have been extensively investigated using response inhibition tasks, such as stop-signal (Logan and Cowan, 1984) and go/nogo tasks (Donders, 1969). In these tasks, prepotent or ongoing actions must be inhibited in response to infrequent signals (Aron, 2011; Bari and Robbins, 2013). The onset of the stop-signal differs between the two tasks: while the nogo-signal is presented instead of or simultaneously with the go-signal in the go/nogo task, the stop-signal in the stop-signal task is presented at some delay after the go signal. The two tasks thus capture different subcomponents of response inhibition, i.e., action restraint and action cancellation, respectively (Schachar et al., 2007). Nevertheless, neuroimaging studies yielded converging evidence of overlapping neural networks during response inhibition tasks (Levy and Wagner, 2011; Swick et al., 2011; Sebastian et al., 2013; Cieslik et al., 2015). This shared stopping network comprises the right inferior frontal gyrus (IFG) and anterior insula, the presupplementary motor area (pre-SMA), and basal ganglia [subthalamic nucleus (STN) and striatum; Duann et al., 2009; Aron, 2011; Levy and Wagner, 2011; Aron et al., 2014; Sebastian et al., 2016]. STN involvement has mainly been discussed in action cancellation, but has also been demonstrated to be implicated in action restraint (Ballanger et al., 2009; Georgiev et al., 2016; Marmor et al., 2020).


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    https://www.psychologytoday.com/us/b...predictability

    https://www.cell.com/neuron/fulltext...273(20)30853-9

    As events in the world unfold, the brain rapidly adjusts its predictions of what will happen next. Of course, our predictions are not always correct—and when they are inaccurate, we often experience surprise (i.e., unsigned prediction error [PE]) (Jang et al., 2019; Kutas and Hillyard, 1984; O’Reilly et al., 2013; Rouhani et al., 2018, Rouhani et al., 2020). Surprise is theorized to be critical for learning and memory (Rescorla and Wagner, 1972; Sinclair and Barense, 2018), updating our beliefs about the structure of the world (Sutton and Barto, 1998), and demarcating events in the continuous flow of time (Franklin et al., 2020).

    [...]

    Our findings reveal that the popular activity of competitive sports viewing is an example of naturalistic surprise, and our analyses of this task led to multiple behavioral and physiological discoveries in support of the tenets of EST (Franklin et al., 2020; Zacks et al., 2011). Namely, surprises appear to strongly coincide with the segmentation of internal event representations, indexed by increased subjective perception of event boundaries, increased pupil dilation, an increased likelihood of significant neural representational shifts (as measured using a HMM), and increased subsequent memory for events.

    Further results provide evidence for reinforcement learning models of RPEs in a naturalistic, passive-viewing setting. In the NAcc, we observed a trend toward classic RPE (signed surprise) effects, reflecting dynamic changes in the probability that a preferred team would win a basketball game (Cikara et al., 2011). In the VTA, we also found classic RPE effects, as well as activity correlated with unsigned updating of beliefs, extending previous work on the VTA to a naturalistic setting (Howard and Kahnt, 2018; Sharpe et al., 2017; Starkweather et al., 2017, Starkweather et al., 2018; Takahashi et al., 2017). Finally, in showing that surprise correlates with subjective enjoyment, we provide support for the intriguing idea that when information is not instrumental for survival, humans may prefer unpredictable scenarios (Ely et al., 2015; Geana et al., 2016).

    Importantly, our approach illustrates a dissociation of surprise effects based on whether they bolstered or contradicted the predominant belief in who would win. Belief-inconsistent surprise—which also leads to a game state of higher uncertainty (Nassar et al., 2019; Shin and DuBrow, 2020)—was a significantly better predictor of subjective event boundaries than belief-consistent surprise. Furthermore, transitions between neural states in precuneus and mPFC were significantly correlated with belief-inconsistent surprise, but not belief-consistent surprise, and the correlation with belief-inconsistent surprise was larger than the correlation with belief-consistent surprise for both regions. Contrary to our results showing a distinction between belief-inconsistent and belief-consistent surprise, measures such as pupil dilation, activity in VTA, and memory showed significant or trending effects for both belief-consistent surprise and belief-inconsistent surprise. Ultimately, different flavors of surprise have different behavioral, physiological, and neural outcomes, demonstrating that individuals’ predictions may have both a binary aspect (i.e., which team will win?) and a probabilistic one (i.e., how likely is it?) (Johnson et al., 2020). These discrepancies raise questions about how and where these two putative aspects of predictions diverge, opening avenues for future research.

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    https://onlinelibrary.wiley.com/doi/...111/tops.12292

    The Cognitive-Evolutionary Model of Surprise: A Review of the Evidence

    Research on surprise relevant to the cognitive-evolutionary model of surprise proposed by Meyer, Reisenzein, and Schützwohl (1997) is reviewed. The majority of the assumptions of the model are found empirically supported. Surprise is evoked by unexpected (schema-discrepant) events and its intensity is determined by the degree if schema-discrepancy, whereas the novelty and the valence of the eliciting events probably do not have an independent effect. Unexpected events cause an automatic interruption of ongoing mental processes that is followed by an attentional shift and attentional binding to the events, which is often followed by causal and other event analysis processes and by schema revision. The facial expression of surprise postulated by evolutionary emotion psychologists has been found to occur rarely in surprise, for as yet unknown reasons. A physiological orienting response marked by skin conductance increase, heart rate deceleration, and pupil dilation has been observed to occur regularly in the standard version of the repetition-change paradigm of surprise induction, but the specificity of these reactions as indicators of surprise is controversial. There is indirect evidence for the assumption that the feeling of surprise consists of the direct awareness of the schema-discrepancy signal, but this feeling, or at least the self-report of surprise, is also influenced by experienced interference. In contrast, facial feedback probably does contribute substantially to the feeling of surprise and the evidence for the hypothesis that surprise is affected by the difficulty of explaining an unexpected event is, in our view, inconclusive. Regardless of how the surprise feeling is constituted, there is evidence that it has both motivational and informational effects. Finally, the prediction failure implied by unexpected events sometimes causes a negative feeling, but there is no convincing evidence that this is always the case, and we argue that even if it were so, this would not be a sufficient reason for regarding this feeling as a component, rather than as an effect of surprise.

    [...]

    It is assumed that, if the schema-discrepancy signal exceeds a certain threshold, then ongoing information processing is automatically (unintentionally) and inevitably interrupted, central resources are reallocated to (i.e., attention is shifted to) the unexpected event, and the unexpectedness signal becomes conscious as a feeling with a characteristic phenomenal quality and intensity: the feeling of surprise. These processes—interruption, attentional shift, and the occurrence of the feeling of surprise—serve to enable and instigate effortful processes of event analysis plus, if this analysis suggests so, immediate reactions to the unexpected event and/or an updating of the beliefs or schemas that gave rise to the schema discrepancy. In more detail, it is assumed that the interruption of processing and the subsequent shift of attention to the unexpected event enable and prepare the ensuing event analysis (by freeing cognitive resources and reallocating these to the unexpected event), whereas the feeling of surprise serves to communicate the occurrence of the schema discrepancy system-wide (see Oatley & Johnson-Laird, 1987) and to provide a motivational impetus for the analysis of the unexpected event, by eliciting curiosity about its nature and causes.




    https://www.cell.com/neuron/fulltext...273(20)30853-9

    In addition to considering enjoyment across a full game, we also investigated the neural effects of surprise on a shorter timescale. Reward signals are intimately linked with the activity of dopamine neurons in regions of the brainstem such as the ventral tegmental area (VTA), as well as targets of those neurons, particularly the nucleus accumbens (NAcc). Classically, the VTA (D’Ardenne et al., 2008; Schultz et al., 1997) and NAcc (Cikara et al., 2011; Gold et al., 2019; Rutledge et al., 2010) respond strongly when rewards are larger or earlier than expected (i.e., reward prediction errors [RPEs]). However, the VTA can respond more broadly to variables other than reward (Engelhard et al., 2019), including sensory PEs (Howard and Kahnt, 2018; Iglesias et al., 2013; Takahashi et al., 2017), unexpected events (Barto et al., 2013; Kafkas and Montaldi, 2015), aversive PEs (Matsumoto et al., 2007), changes in hidden belief states (Nour et al., 2018; Starkweather et al., 2018), reward expectation (Kim et al., 2016; Totah et al., 2013), advance information (Bromberg-Martin and Hikosaka, 2011), and stimulus-stimulus learning (Sharpe et al., 2017), all in the absence of (or controlling for) reward.




    https://abcnews.go.com/Health/story?id=116829&page=1

    Apparently the brain's pleasure centers are more "turned on" when we experience unpredictable pleasant things, compared to expected pleasant events, according to new pictures of the brain responding to surprises.

    [...]

    "This means that the brain finds unexpected pleasure more rewarding that expected ones, and it may have little to do with what people say they like," said Dr. Gregory Berns, assistant professor of biomedical engineering at Emory and Dr. Read Montague, associate professor of neuroscience at Baylor, the authors of the study.

    ------

    Surprise is not directly linked to motivation ('wanting').

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    the feeling of surprise serves to communicate the occurrence of the schema discrepancy system-wide (see Oatley & Johnson-Laird, 1987)
    yes



    and to provide a motivational impetus for the analysis of the unexpected event, by eliciting curiosity about its nature and causes.
    no, this is interest (---> a potential reward)

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    contempt: You should be ashamed of yourself!

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    https://www.ulm.edu/~palmer/Box%207_prideandshame.htm

    Darwin (1872) noted that expressions of pride and shame in humans parallel the signals for dominance and submission displayed by other species.

    Weisfeld (1999) makes a compelling argument that the terms shame and pride can be used to subsume a plethora of divergent psychological constructs such as self-esteem, guilt, prestige striving, success striving, social comparison, approval motivation, prosocial behavior and a multitude of others.

    Pride and shame appear to be mediated at the proximate physiological level by an area of the brain called the orbitofrontal cortex (Carlson, 1998).

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    Wikipedia

    The anterior cingulate cortex is central to the affective response of physical pain and is involved in the detection and interpretation of social pain such as threats, rejection, exclusion, loss, and negative evaluation of others. The anterior cingulate cortex is particularly active when the individual thinks negative thoughts about himself.


    https://www.jneurosci.org/content/31/25/9307

    The subgenual anterior cingulate cortex (sgACC) has been shown to encode both positive and negative values (Blood et al., 1999; Plassmann et al., 2010).



    https://www.nature.com/articles/s41583-022-00589-2

    Individual orbitofrontal cortex (OFC) neurons typically encode the value of the chosen picture.

    ------

    ACC and OFC <--> value

    1. happiness and sadness

    2. pride and shame

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