CARE <--> social grooming
PLAY <--> play fighting
CARE <--> social grooming
PLAY <--> play fighting
I think this is social grooming rather than play fighting.https://www.npr.org/2021/05/22/99949...oo-study-shows
MARTIN: That is a kea, a species of parrot native to New Zealand. And what we heard was its way of saying, relax, we're only playing around.
SASHA WINKLER: The main reason why you need play signals is that this helps disambiguate, saying this is play versus I'm actually biting you in the neck.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9014270/
Response Flexibility: The Role of the Lateral Habenula
The ability to make appropriate decisions that result in an optimal outcome is critical for survival. This process involves assessing the environment as well as integrating prior knowledge about the environment with information about one’s current internal state. There are many neural structures that play critical roles in mediating these processes, but it is not yet known how such information coalesces to influence behavioral output. The lateral habenula (LHb) has often been cited as a structure critical for adaptive and flexible responding when environmental contexts and internal state changes. A challenge, however, has been understanding how LHb promotes response flexibility. In this review, we hypothesize that the LHb enables flexible responding following the integration of context memory and internal state information by signaling downstream brainstem structures known to drive hippocampal theta. In this way, animals respond more flexibly in a task situation not because the LHb selects a particular action, but rather because LHb enhances a hippocampal neural state that is often associated with greater attention, arousal, and exploration. In freely navigating animals, these are essential conditions that are needed to discover and implement appropriate alternative choices and behaviors. As a corollary to our hypothesis, we describe short- and intermediate-term functions of the LHb. Finally, we discuss the effects on the behavior of LHb dysfunction in short- and intermediate-timescales, and then suggest that new therapies may act on the LHb to alleviate the behavioral impairments following long-term LHb disruption.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5659956/
Subjective decisions, such as those made between small immediate rewards and larger but delayed rewards in delay discounting tasks, reveal contributions to choice behavior when either choice may be considered “correct”. This allows for the separation of choice from objective errors or aversive (no reward) experiences. When the LHb is inactivated, delay discounting performance drops to chance levels even at short delays (Stopper and Floresco 2014). This surprising result indicates that the LHb contributes to choice behavior even when there is no objectively correct choice. In risk based decisions in which the larger reward is instead given at increasingly less frequent probabilities across the session, LHb inactivation also led to similar chance performance (Stopper and Floresco 2014). Interestingly, if the small and large rewards are directly compared with no time delay or probability of receiving the reward, rats were able to discriminate similarly to controls. These findings demonstrate that the role of the LHb in subjective decisions is not primarily to signal reward (or aversive) outcomes to guide future decisions. Rather, these data suggest that the LHb is required when the animal must track a learned strategy or choice pattern as it changes across the session based on the current delay or probability of the large reward. This is another example of evidence that supports a broad and more fundamental role for the LHb in tasks that require flexible responses.
A little girl falls and starts crying.
I don't think this is sadness. Sadness is most likely a mood (not an emotion).
happiness and sadness <--> coping, overcoming stress
(see post #3)
https://www.sciencedirect.com/scienc...06322322015943
The mu opioid receptor (MOR) is central to hedonic balance and produces euphoria by engaging reward circuits. MOR signaling may also influence aversion centers, notably the habenula (Hb), where the receptor is highly dense. Our previous data suggest that the inhibitory activity of MOR in the Hb may limit aversive states. To investigate this hypothesis, we tested whether neurons expressing MOR in the Hb (Hb-MOR neurons) promote negative affect.
https://www.sciencedirect.com/topics...ience/euphoria
The euphoria associated with many classes of addictive drugs is thought to involve the stimulation of opioid receptors (for review see Koob & Le Moal, 2001). Chronic self-administration of heroin increases μ opioid receptor (MOR) binding in the VTA, NAc, caudate putamen, and hippocampus (Fattore et al., 2007).
https://www.ncbi.nlm.nih.gov/books/NBK546642/
The mu-2 receptor is vital for euphoria, dependence...
https://medlineplus.gov/genetics/gene/oprm1/
The μ opioid receptor was the first opioid receptor to be discovered. It is the primary receptor for endogenous opioids called beta-endorphin and enkephalins, which help regulate the body's response to pain, among other functions. The μ opioid receptor is also the binding site for many opioids introduced from outside the body (called exogenous opioids). These include commonly prescribed pain medications such as oxycodone, fentanyl, buprenorphine, methadone, oxymorphone, hydrocodone, codeine, and morphine, as well as illegal opioid drugs such as heroin.
When endogenous or exogenous opioids bind to the μ opioid receptor, the interaction triggers a cascade of chemical signals in the nervous system. These signals reduce the activity (excitability) of neurons in certain areas of the brain, which leads to pain relief and feelings of pleasure and intense happiness (euphoria). In addition, the chemical signaling ultimately increases the production of a chemical called dopamine. Dopamine is a chemical messenger (neurotransmitter) that helps regulate areas of the brain involved in reward-seeking behavior, attention, and mood.
https://link.springer.com/article/10...15-021-00960-3
μ-opioid receptor availability is associated with sex drive in human males
Opioid receptors (OR) are widely expressed in the neurocircuitry that underlies sexual behavior (Le Merrer et al., 2009). Yet, the exact role of OR agonists and antagonists in exciting and inhibiting sexual behaviors is complex with nuanced differences across species and conditions. In a fashion similar to that of having sex, opioid agonists may increase pleasure and liking, and the euphoric sensations following opioid administration in drug addicts has sometimes been called “pharmacogenic orgasm” (Chessick, 1960).
https://www.goodtherapy.org/blog/psychpedia/euphoria
Euphoria is an overwhelming feeling of happiness, joy, and well-being. People experiencing euphoria may feel carefree, safe, and free of stress. This emotion can be either a normal reaction to happy events or a symptom of substance abuse and certain mental health conditions.
Euphoria and Neurotransmitters
Dopamine is the primary neurotransmitter responsible for euphoria. This chemical enables feelings of pleasure and well-being, and insufficient quantities of dopamine can inhibit a person’s ability to feel pleasure. Serotonin can also affect feelings of well-being, although serotonin does not typically cause feelings of euphoria. Medications that regulate neurotransmitters can enable people to feel satisfaction and happiness, as well as more elated feelings of euphoria.
Last edited by Petter; 06-18-2023 at 07:39 AM.
1. food and well-being (exercise and social activities) ---> survival ... reward: pleasure ('liking'), maybe euphoria
2. sex ---> reproduction ... reward: pleasure ('liking'), maybe euphoria
3. a threat ---> survival ... punishment: pain, discomfort or disgust
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improve 1, 2 or 3 ... reward: euphoria, happiness
habenula: emotion + context (=meaningfulness)
habenula.jpg
"What receptors are responsible for euphoria?
Euphoria is mediated by μ receptors. Activation of κ receptors produces dysphoria."
https://en.wikipedia.org/wiki/%CE%9A-opioid_receptor
The κ-opioid receptor or kappa opioid receptor, abbreviated KOR or KOP for its ligand ketazocine, is a G protein-coupled receptor that in humans is encoded by the OPRK1 gene. The KOR is coupled to the G protein Gi/G0 and is one of four related receptors that bind opioid-like compounds in the brain and are responsible for mediating the effects of these compounds. These effects include altering nociception, consciousness, motor control, and mood. Dysregulation of this receptor system has been implicated in alcohol and drug addiction.
https://www.sciencedirect.com/topics...pioid-receptor
Activation of the κ opioid receptor decreases dopamine levels and leads to dysphoria.
https://www.nature.com/articles/s41386-018-0225-3
see figure 2
Last edited by Petter; 06-19-2023 at 07:23 AM.
https://www.frontierspartnerships.or...021.10009/full
Research in the field of affective neuroscience suggests that separation distress represents one of the ancestral primary-process emotional systems (referred to as PANIC/GRIEF). Importantly, the PANIC/GRIEF system probably evolved from general pain mechanisms, and studies have found a link between separation distress and physical pain.
[...]
The neuroanatomy of the PANIC/GRIEF system overlaps with the brain’s system for processing physical pain, suggesting that both physically painful (e.g., injury) and emotionally painful (e.g., interpersonal rejection) stimuli may engage this shared neurocircuitry to produce distress and dysphoria (emotional pain), with separation distress representing a particular subtype of emotional pain.
https://www.researchgate.net/figure/...fig1_328414168
wanting and liking circuitry.png
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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).
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https://sites.lsa.umich.edu/berridge...oyful-mind.pdf
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https://psywb.springeropen.com/artic.../2211-1522-1-3
Sensory pleasures: From sensation to 'liking' to hedonic feelings
First, what is pleasure? Pleasure is never merely a sensation, even for sensory pleasures (Frijda 2010; Katz, 2006; Kringelbach 2010; Kringelbach and Berridge 2010; Ryle 1954). Instead it always requires the recruitment of specialized pleasure-generating brain systems to actively paint an additional "hedonic gloss" onto a sensation. Active recruitment of brain pleasure-generating systems is what makes a pleasant experience 'liked'.
The capacity of certain stimuli, such as a sweet taste or a loved one, to reliably elicit pleasure -- to nearly always be painted with a hedonic gloss -- reflects the privileged ability of such stimuli to activate those hedonic brain systems responsible for manufacturing and applying the gloss. Hedonic brain systems are well-developed in the brain, spanning subcortical and cortical levels, and are quite similar across humans and other animals.
Some might be surprised by high similarity across species, or by substantial subcortical contributions, at least if one thinks of pleasure as uniquely human and as emerging only at the top of the brain. The neural similarity indicates an early phylogenetic appearance of neural circuits for pleasure and a conservation of those circuits, including deep brain circuits, in the elaboration of later species, including humans. Substantial mechanisms for pleasure would be selected and conserved only if they ultimately served a central role in fulfilling Darwinian imperatives of gene proliferation via improved survival and procreation, suggesting the capacity for pleasure must have been fundamentally important in evolutionary fitness (Berridge and Schulkin 1989; Cabanac 2010; Darwin 1872; Nesse 2002; Panksepp 1998; Rolls 2005; Schulkin 2004; Tindell et al. 2006).
Pleasure as an adaptive evolutionary feature is not so hard to imagine. For example, tasty food is one of the most universal routes to pleasure, as well as an essential requirement to survival. Not accidentally, food is also is one of the most accessible experimental methods available to psychology and neuroscience studies of pleasure (Berridge et al. 2010; Gottfried 2010; Kringelbach 2005; Kringelbach and Berridge 2010; Peciña Smith and Berridge, 2006; Rozin 1999; Veldhuizen et al. 2010). Much of what we will say here comes from such studies.
Beyond food, sex is another potent and adaptive sensory pleasure which involves some of the same brain circuits (Geogiadis and Kortekaas 2010; Komisaruk et al. 2010). Many other special classes of stimuli also appear tap into the same limbic circuits. Even rewarding drugs of abuse are widely viewed to hijack the same hedonic brain systems that evolved to mediate food, sex and other natural sensory pleasures (Everitt et al. 2008; Kelley and Berridge 2002; Koob and Volkow 2010).
Another fundamental pleasure is social interaction with conspecifics, which draws on overlapping neural systems and is important even from an evolutionary perspective (Aragona et al. 2006; Britton et al. 2006; Frith and Frith 2010; King-Casas et al. 2005; Kringelbach et al. 2008; Leknes and Tracey 2008). In fact, it might well be that in humans, at least, the social pleasures are often as pleasurable as the basic sensory pleasures.
Most uniquely, humans have many prominent higher order, abstract or cultural pleasures, including personal achievement as well as intellectual, artistic, musical, altruistic, and transcendent pleasures. While the neuroscience of higher pleasures is in relative infancy, even here there seems overlap in brain circuits with more basic hedonic pleasures (Frijda 2010; Harris et al. 2009; Leknes and Tracey 2010; Salimpoor et al. 2011; Skov 2010; Vuust and Kringelbach 2010). As such, brains may be viewed as having conserved and re-cycled some of the same neural mechanisms of hedonic generation for higher pleasures that originated early in evolution for simpler sensory pleasures.
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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3008658/
A related but slightly different view is that happiness depends most chiefly on eliminating negative “pain and displeasure” to free an individual to pursue engagement and meaning. Positive pleasure by this view is somewhat superfluous. This view may characterize the twentieth-century medical and clinical emphasis on alleviating negative psychopathology and strongly distressing emotions. It fits also with William James’s quip nearly a century ago that “happiness, I have lately discovered, is no positive feeling, but a negative condition of freedom from a number of restrictive sensations of which our organism usually seems the seat. When they are wiped out, the clearness and cleanness of the contrast is happiness. This is why anaesthetics make us so happy. But don’t you take to drink on that account” (James 1920: 158).
wanting and liking.jpg
Last edited by Petter; 06-23-2023 at 02:50 PM.
This is PANIC/distress/dysphoria (an emotion).A little girl falls and starts crying.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5214632/ (Habenula-Induced Inhibition of Midbrain Dopamine Neurons...)
These results are the first to show that RMTg neurons contribute directly to LHb-induced inhibition of DA cell activity and support the widely held proposition that GABAergic neurons in the mesopontine tegmentum are an important component of a pathway that enables midbrain DA neurons to encode the negative valence associated with failed expectations and aversive stimuli.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2613689/
Habenula: Crossroad between the Basal Ganglia and the Limbic System
There is a growing awareness that emotion, motivation, and reward values are important determinants of our behavior. The habenula is uniquely positioned both anatomically and functionally to participate in the circuit mediating some forms of emotive decision making. In the last few years there has been a surge of interest in this structure, especially the lateral habenula (LHb). The new studies suggest that the LHb plays a pivotal role in controlling motor and cognitive behaviors by influencing the activity of dopamine and serotonin neurons. Further, dysfunctions of the LHb have also been implicated in psychiatric disorders, such as depression, schizophrenia, and drug-induced psychosis.
https://pubmed.ncbi.nlm.nih.gov/31833616/
The habenula (Hb) is a phylogenetically old epithalamic structure differentiated into two nuclear complexes, the medial (MHb) and lateral habenula (LHb). After decades of search for a great unifying function, interest in the Hb resurged when it was demonstrated that LHb plays a major role in the encoding of aversive stimuli ranging from noxious stimuli to the loss of predicted rewards. Consistent with a role as an anti-reward center, aberrant LHb activity has now been identified as a key factor in the pathogenesis of major depressive disorder. Moreover, both MHb and LHb emerged as new players in the reward circuitry by primarily mediating the aversive properties of distinct drugs of abuse. Anatomically, the Hb serves as a bridge that links basal forebrain structures with monoaminergic nuclei in the mid- and hindbrain. So far, research on Hb has focused on the role of the LHb in regulating midbrain dopamine release. However, LHb/MHb are also interconnected with the dorsal (DR) and median (MnR) raphe nucleus. Hence, it is conceivable that some of the habenular functions are at least partly mediated by the complex network that links MHb/LHb with pontomesencephalic monoaminergic nuclei. Here, we summarize research about the topography and transmitter phenotype of the reciprocal connections between the LHb and ventral tegmental area-nigra complex, as well as those between the LHb and DR/MnR. Indirect MHb outputs via interpeduncular nucleus to state-setting neuromodulatory networks will also be commented. Finally, we discuss the role of specific LHb-VTA and LHb/MHb-raphe circuits in anxiety and depression.
https://www.sciencedirect.com/scienc...59438817302908
Figure 1. Summary of the input and output circuitry of the LHb. Projections to the lateral habenula (LHb), shown in brown, include the paraventricular nucleus (PVN), basal forebrain (BF, including the nucleus accumbens (NAc), lateral septum, and diagonal band nuclei (DBN)), lateral hypothalamic area (LHA), lateral preoptic area (LPO), ventral pallidum (VP), globus pallidus (GPi), medial prefrontal cortex (mPFC), suprachiasmatic nucleus (SCN), and bed nucleus of the stria terminalis (BNST). Potential functional role of each input pathway is noted. The references are indicated on the top of the figure. The main output of the LHb, shown in red, is glutamatergic. The LHb neurons preferentially form synapses on GABAergic or dopaminergic neurons in the VTA and substantia nigra pars compacta (SNc), GABAergic or serotoninergic neurons in the dorsal raphe nucleus (DRN) and median raphe nucleus (MSN), as well as GABAergic neurons in the rostromedial tegmental nucleus (RMTg). The GABAergic RMTg inhibits DA and 5HT neurons. The VTA and DRN/MSN also send reciprocal feedback inputs into the LHb.
habenula 3.jpg
http://www.neuwritewest.org/blog/a-n...-of-depression
habenula 4.png
Last edited by Petter; 06-23-2023 at 02:07 PM.
https://www.sciencedirect.com/scienc...32118X15000641
Going with your gut: How William James' theory of emotions brings insights to risk perception and decision making research
The basic premise of William James' theory of emotions – that bodily changes lead to emotional feelings – ignited debate about the relative importance of bodily processes and cognitive appraisals in determining emotions. Similarly, theories of risk perception have been expanding to include emotional and physiological processes along with cognitive processes. Taking a closer look at The Principles of Psychology, this article examines how James' propositions support and extend current research on risk perception and decision making. Specifically, James (1) described emotional feelings and their related cognitions in ways similar to current dual processing models; (2) defended the proposition that emotions and their expressions serve useful and adaptive functions; (3) suggested that anticipating an emotion can trigger that emotion due to associations learned from past experiences; and (4) highlighted individual differences in emotional experiences that map on well with individual differences in risk-related decision making.
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.
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https://www.cell.com/current-biology...18)30917-5.pdf
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https://psu.pb.unizin.org/psych425/c...and-the-brain/
These findings would suggest that for normal functioning individuals, when we experience anger, the OFC helps us to regulate our aggressive approach behaviors.
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OFC.jpg
OFC NAcc motivational behavior.jpg
Last edited by Petter; 06-26-2023 at 05:52 AM.
https://www.frontiersin.org/articles...018.00026/full
FIGURE 1. Mechanisms of glucocorticoid deficit-induced aggression are combinations of those subserving intraspecific and predatory aggressions. For explanations, see section Introduction. Dashed arrows indicate hypothetical information flow. CeA, central amygdala; LH, lateral hypothalamus; MBH, mediobasal hypothalamus (hypothalamic attack area); MeA, medial amygdala; mPFC, medial prefrontal cortex; OFC, orbitofrontal cortex; PAG, periaqueductal gray. Dashed arrows, hypothetical flow of information.
hypothalamus aggression.jpg
(see post #303)
excitement: DA (high) <--> NA (high)
euphoria: DA (high) <--> 5-HT (high)
(see post #45)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4279075/
Serotonin 5-HT2 Receptor Interactions with Dopamine Function: Implications for Therapeutics in Cocaine Use Disorder
https://www.researchgate.net/figure/...fig1_363143461
Illustration showing the interaction of at least seven major neurotransmitter pathways in the complex of the Brain Reward Cascade (BRC). In the hypothalamus, environmental stimulation springs the release of serotonin, which in succession via, for example, 5HT-2a receptors activate (equal green sign) the ensuing release of opioid peptides from opioid peptide neurons, also occurring in the hypothalamus. Afterwards, the opioid peptides have, potentially via two different opioid receptors, two distinct effects: one that inhibits (red hash sign) through the mu-opioid receptor (possibly via enkephalin) and projects to the Substantia Nigra to GABAA neurons; or the other, which stimulates (equal green sign) cannabinoid neurons (the Anandamide and 2-archydonoglcerol, for example) via Beta-Endorphin-linked delta receptors, which in turn inhibit GABAA neurons at the Substantia Nigra. Additionally, when activated, cannabinoids, largely 2-archydonoglcerol, may indirectly disinhibit (red hash sign) GABAA neurons through activation of G1/0 coupled to CB1 receptors in the Substantia Nigra. In the Dorsal Raphe Nuclei, glutamate neurons can indirectly disinhibit GABAA neurons in the Substantia Nigra through activation of GLU M3 receptors (red hash sign). GABAA neurons, when stimulated, will, in turn, intensely (red hash signs) inhibit VTA glutaminergic drive via GABAB 3 neurons. It is also feasible that stimulation of ACH neurons at the Nucleus Accumbens ACH will stimulate muscarinic (red hash) or Nicotinic receptors (green hash). Lastly, Glutamate neurons in the VTA will project to dopamine neurons by way of NMDA receptors (equal green sign) to preferentially release dopamine at the Nucleus Accumbens, depicted as a bullseye which indicates a euphoria or ʺwantingʺ response. The outcome is that when dopamine release is low (endorphin deficiency), unhappiness is experienced, while general (healthy) happiness is dependent on the dopamine homeostatic tonic set point. (With permission from Blum et al.) [20].
dopamine serotonin euphoria 2.jpg
Last edited by Petter; 06-27-2023 at 04:27 AM.
https://nida.nih.gov/publications/dr...on/drugs-brainhttps://en.wikipedia.org/wiki/Reward...easure_centers
Pleasure is a component of reward, but not all rewards are pleasurable (e.g., money does not elicit pleasure unless this response is conditioned). Stimuli that are naturally pleasurable, and therefore attractive, are known as intrinsic rewards, whereas stimuli that are attractive and motivate approach behavior, but are not inherently pleasurable, are termed extrinsic rewards. Extrinsic rewards (e.g., money) are rewarding as a result of a learned association with an intrinsic reward. In other words, extrinsic rewards function as motivational magnets that elicit "wanting", but not "liking" reactions once they have been acquired.
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. The hotspot within the nucleus accumbens shell is located in the rostrodorsal quadrant of the medial shell, while the hedonic coldspot is located in a more posterior region. The posterior ventral pallidum also contains a hedonic hotspot, while the anterior ventral pallidum contains a hedonic coldspot. In rats, microinjections of opioids, endocannabinoids, and orexin are capable of enhancing liking reactions in these hotspots. The hedonic hotspots located in the anterior OFC and posterior insula have been demonstrated to respond to orexin and opioids in rats, as has the overlapping hedonic coldspot in the anterior insula and posterior OFC. On the other hand, the parabrachial nucleus hotspot has only been demonstrated to respond to benzodiazepine receptor agonists.
Hedonic hotspots are functionally linked, in that activation of one hotspot results in the recruitment of the others, as indexed by the induced expression of c-Fos, an immediate early gene. Furthermore, inhibition of one hotspot results in the blunting of the effects of activating another hotspot. Therefore, the simultaneous activation of every hedonic hotspot within the reward system is believed to be necessary for generating the sensation of an intense euphoria.
Pleasure or euphoria—the high from drugs—is still poorly understood, but probably involves surges of chemical signaling compounds including the body’s natural opioids (endorphins) and other neurotransmitters in parts of the basal ganglia (the reward circuit). When some drugs are taken, they can cause surges of these neurotransmitters much greater than the smaller bursts naturally produced in association with healthy rewards like eating, hearing or playing music, creative pursuits, or social interaction.
It was once thought that surges of the neurotransmitter dopamine produced by drugs directly caused the euphoria, but scientists now think dopamine has more to do with getting us to repeat pleasurable activities (reinforcement) than with producing pleasure directly.
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'wanting' <--> excitement, interest
'liking' <--> euphoria
5 basic emotions
excitement, interest <--> a potential reward
anger, annoyance <--> a potential reward and a potential punishment
fear, nervousness <--> a potential punishment
euphoria, enjoyment <--> a reward/pleasure or a lack of punishment/pain
dysphoria <--> a punishment or a lack of reward
... or less punishment/pain (an improvement)euphoria, enjoyment <--> a reward/pleasure or a lack of punishment/pain
https://pubmed.ncbi.nlm.nih.gov/32220099/
"Feeling high" and "feeling happy" were associated with pain improvement (p < 0.01) but not with hydromorphone administration (p = 0.07 for "high" and p = 0.06 for "happy"). Medication-induced side effects were not associated with these measures of euphoria.
https://www.sciencedirect.com/scienc...6192307890014X
Reduction of distress vocalization in chicks by opiate-like peptides ... PANKSEPP, J. et al.
Reduction of distress vocalization in chicksby opiate-like peptides. BRAIN RES. BULL. 3(6) 663–667, 1978.—All the opiate-like peptides we tested (Met-enkephalin, (D-Ala2)-Met-enkaphalin-NH2, β-endorphin, (D-Ala2)-β-endorphin, (D-Ala2)-α-endorphin, (D-Ala2)-γ-endorphin) were capable of reducing distress vocalizations (DV's) in socially-isolated chicks when injected into the vicinity of the fourth ventricle in doses as low as 100 picomoles. All of these substances were at least as potent as equimolar doses of morphine sulfate. In general, DV's were a more sensitive measure of opiate-like peptide effects than reductions in body temperature. In a more limited study using peripheral injections, it was determined that (D-Ala2)-Met-enkephalin at doses of 400 nanomoles/kg, like morphine sulfate, was more effective in reducing DV's, than an equimolar dose of β-endorphin. β-endorphin was not as effective via a peripheral route as it was via central administration.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181986/
Affective neuroscience of the emotional BrainMind: evolutionary perspectives and implications for understanding depression ... Jaak Panksepp
Brain research supports the existence of at least seven primary-process (basic) emotional systems - SEEKING, RAGE, FEAR, LUST, CARE, GRIEF (formerly PANIC), and PLAY - concentrated in ancient subcortical regions of all mammalian brains.
In sum, affective neuroscientific analysis of basic emotions is based on several highly replicable facts: (i) Coherent emotional-instinctual behaviors can be aroused by electrically stimulating very specific subcortical regions of the brain; (ii) Wherever one evokes emotional action patterns with ESB, there are accompanying affective experiences. Again, the gold standard for this assertion is the fact that the brain stimulations can serve as “rewards” when positive-emotions are aroused - eg, SEEKING, LUST, CARE, and aspects of PLAY. When negative emotions are aroused - RAGE, FEAR, GRIEF - animals escape the stimulation; (iii) The above behavioral and affective changes are rarely, if ever, evoked from higher prefrontal neocortical regions, suggesting that higher brain areas may not have the appropriate circuitry to generate affective experiences, although the neocortex can clearly regulate (eg, inhibit) emotional arousals and, no doubt, prompt emotional feelings by dwelling on life problems.
The SEEKING/desire system
This extensive network confluent with the medial forebrain bundle (MFB) is traditionally called the “brain reward system.” In fact, this is a general-purpose appetitive motivational system that is essential for animals to acquire all resource needs for survival, and it probably helps most other emotional systems to operate effectively. It is a major source of life “energy”, sometimes called “libido.” In pure form, it provokes intense and enthusiastic exploration and appetitive anticipatory excitement/learning. When fully aroused, SEEKING fills the mind with interest and motivates organisms to effortlessly search for the things they need, crave, and desire. In humans, this system generates and sustains curiosity from the mundane to our highest intellectual pursuits. This system becomes underactive during addictive drug withdrawal, chronic stress, and sickness, and with accompanying feelings of depression. Overactivity of this system can promote excessive and impulsive behaviors, along with psychotic delusions and manic thoughts. All antipsychotics reduce arousability of this “reality-creating” mechanism of the brain. The term “reality-creating” is used to highlight the fact that this system appears to generate causal convictions about the nature of the world from the perception of correlated events (for a full discussion see Chapter 8 of Affective Neuroscience 3).
Neuroanatomically, SEEKING circuitry corresponds to the extensive medial forebrain bundle and major dopamine-driven, self-stimulation “reward” circuitry coursing from ventral midbrain to nucleus accumbens and medial frontal cortex, where it can promote frontal cortical functions related to planning and foresight. Rather than being a “pleasure or reinforcement system,” SEEKING coaxes animals to acquire resources needed for survival. It promotes learning by mediating anticipatory eagerness, partly by coding predictive relationships between events. It promotes a sense of engaged purpose in both humans and animals, and is diminished in depression and the dysphoria of withdrawal from addictive drugs. This is further highlighted by the simple fact that bilateral lesions of the system produce profound amotivational states in animals (all appetitive behaviors are diminished) and the elevated threshold for self-stimulation reward probably reflects the dysphoria state.
The RAGE/anger system
When SEEKING is thwarted, RAGE is aroused. Anger is provoked by curtailing animals' freedom of action. RAGE is a reliably provoked ESB of a neural network extending from the medial amygdala and hypothalamus to the dorsal PAG. RAGE lies close to and interacts with trans-diencephalic FEAR systems, highlighting the implicit source of classic “fight-flight” terminology. It invigorates aggressive behaviors when animals are irritated or restrained, and also helps animals defend themselves by arousing FEAR in their opponents. Human anger may get much of its psychic energy from the arousal of this brain system; ESB of the above brain regions can evoke sudden, intense anger attacks, with no external provocation. Key chemistries which arouse this system are the neuropeptide Substance P and glutamate, while endogenous opioids and y-aminobutyric acid (GABA) inhibit the system. A prediction is that glutamate and Substance P receptor antagonists (eg, aprepitant) may help control human anger. Additional medicines to control RAGE could presumably be developed through further detailed understanding of RAGE circuitry.
The FEAR/anxiety system
The evolved FEAR circuit helps to unconditionally protect animals from pain and destruction. FEAR-ESB leads animals to flee, whereas much weaker stimulation elicits a freezing response. Humans stimulated in these same brain regions report being engulfed by an intense free-floating anxiety that appears to have no environmental cause. Key chemistries that regulate this system are Neuropeptide Y and corticotrophin releasing factor (CRF); anti-anxiety agents such as the benzodiazepines inhibit this system by facilitating GABA transmission.
The LUST/sexual systems
Sexual LUST, mediated by specific brain circuits and chemistries, distinct for males and females, is aroused by male and female sex hormones, which control many brain chemistries including two “social neuropeptides” - oxytocin transmission is promoted by estrogen in females and vasopressin transmission by testosterone in males. These brain chemistries help create gender-specific sexual tendencies. Oxytocin promotes sexual readiness in females, as well as trust and confidence, and vasopressin promotes assertiveness, and perhaps jealous behaviors, in males. Distinct male and female sexual tendencies are promoted by these steroid hormones early in life, with sexual activation by gonadal hormones at puberty. Because brain and bodily sex characteristics are independently organized, it is possible for animals that are externally male to have female-typical sexual urges and, others with female external characteristics to have maletypical sexual urges. The dopamine-driven SEEKING system participates in the search for sexual rewards just as for all other types of rewards, including those relevant for the other social-emotional systems described below.
The CARE/maternal nurturance system
Brain evolution has provided safeguards to assure that parents (usually the mother) take care of offspring. Some of the chemistries of sexuality, for instance oxytocin, have been evolutionarily redeployed to mediate maternal care - nurturance and social bonding - suggesting there is an intimate evolutionary relationship between female sexual rewards and maternal motivations.29 The shifting hormonal tides at the end of pregnancy (declining progesterone, and increasing estrogen, prolactin, and oxytocin) invigorate maternal urges days before the young are born. This collection of hormonal and associated neurochemical changes also help assure strong maternal bonds with offspring.
The GRIEF/separation distress system
[This] system was initially called the PANIC system, but few understood the intent of that primary-process terminology, so we shifted to the more comprehensible tertiary-process term of GRIEF (highlighting once more terminological problems in emotion research: what are the differences between the tertiary-level emotions of bereavement, grief, and mourning, for instance?). In any event, young socially dependent animals have powerful emotional systems to solicit nurturance. They exhibit intense crying when lost, alerting caretakers to attend to their offspring. ESB mapping of this separation-distress system has highlighted circuitry running from dorsal PAG to anterior cingulate, and it is aroused by glutamate and CRF and inhibited by endogenous opioids, oxytocin, and prolactin - the major social-attachment, socialbonding chemistries of the mammalian brain. These neurochemicals are foundational for the secure attachments that are so essential for future mental health and happiness. It is still worth considering that panic attacks may reflect sudden endogenous spontaneous loss of feelings of security (acute separation-distress) rather than sudden FEAR. We predict that these circuits are tonically aroused during human grief and sadness, feelings that accompany low brain opioid activity.
The PLAY/rough-and-tumble, physical socialengagement system
Young animals have strong urges for physical play - running, chasing, pouncing, and wrestling. These “aggressive” - assertive actions are consistently accompanied by positive affect - an intense social joy - signaled in rats by making abundant high frequency (~50 kHz) chirping sounds, resembling laughter. One key function of social play is to learn social rules and refine social interactions. Subcortically concentrated PLAY urges may promote the epigenetic construction of higher social brain functions, including empathy. Further studies of this system may lead to the discovery of positive affect promoting neurochemistries that may be useful in treating depression.
LUST, CARE, GRIEF and PLAY could be seen as one basic emotional system (<--> euphoria/dysphoria).
Categorical versus Dimensional Models of Affect: A seminar on the theories of Panksepp and Russell
"A key function of the social play system is to facilitate the natural emergence of social dominance. Play helps young animals to acquire more subtle social interactions that are not genetically coded into the brain but must be learned. Thus, the play urge may be one of the major emotional forces that promotes the epigenetic construction of higher social brains - promoting humor and teasing in humans."
excitement, interest <--> work towards a goal
anger, annoyance <--> fight (an enemy or an obstacle)
fear, nervousness <--> freeze or flight (a threat)
euphoria, enjoyment <--> leisure
dysphoria <--> recuperation
https://emotiontypology.com/positive...on/excitement/
The evolutionary function of excitement may be to promote exploratory behavior. It causes you to focus your attention on something good that will in the future, so you don’t miss the opportunity. Another function of excitement may be to shift your focus from potential risks to the potential benefits of anticipated events, leading to more impulsive or risk-taking behavior. Evolutionary, people in many cases may have benefitted from playing it safe, but in the face of high potential rewards, it can be very beneficial to take more risks.
https://en.wikipedia.org/wiki/Habenu..._and_addiction
LHb is especially important in understanding the reward and motivation relationship as it relates to addictive behaviors. The LHb inhibits dopaminergic neurons, decreasing the release of dopamine. It was determined by several animal studies that receiving a reward coincided with elevated dopamine levels, but once the learned association was learned by the animal, dopamine levels remain elevated, only decreasing when the reward is removed. Therefore, dopamine levels only increase with unpredicted rewards and with a "positive prediction error". Moreover, it was determined that removal of an anticipated award activated LHb, inhibited dopamine levels. This finding helps explain why addictive drugs are associated with elevated dopamine levels.
https://neurosciencenews.com/lateral...-reward-21337/
A tiny but important area in the middle of the brain acts as a switch that determines when an animal is willing to work for a reward and when it stops working, according to a study published Aug. 31 (2022) in the journal Current Biology.
https://www.sciencedirect.com/scienc...66432815002600
Dopamine neurons located in the midbrain play a role in motivation that regulates approach behavior (approach motivation). In addition, activation and inactivation of dopamine neurons regulate mood and induce reward and aversion, respectively. Accumulating evidence suggests that such motivational role of dopamine neurons is not limited to those located in the ventral tegmental area, but also in the substantia nigra. The present paper reviews previous rodent work concerning dopamine's role in approach motivation and the connectivity of dopamine neurons, and proposes two working models: One concerns the relationship between extracellular dopamine concentration and approach motivation. High, moderate and low concentrations of extracellular dopamine induce euphoric, seeking and aversive states, respectively. The other concerns circuit loops involving the cerebral cortex, basal ganglia, thalamus, epithalamus, and midbrain through which dopaminergic activity alters approach motivation. These models should help to generate hypothesis-driven research and provide insights for understanding altered states associated with drugs of abuse and affective disorders.
https://www.jimhopper.com/pdf/alcaro...11_seeking.pdf
This SEEKING disposition (for short) is characterized by (i) overt behavioral responses (exploration, seeking and approaching), (ii) by memory and cognitive effects (’reinforcement’ of associative learning, activation of contextual memories and anticipatory predictions) and by (iii) specific kinds of positive affective feelings (a generalized incentive ‘emotional’ reward state, that does not reflect the pleasure of sensation, but rather the euphoria of appetitive eagerness).
[...]
But there is every indication that these “parts” work in a coordinated fashion to generate a unified emotional drive, accompanied by an exploratory behavioral urge and energized-euphoric feelings. In our view, not only does this system mediate a positive euphoric feeling quite different from sensory pleasures...
[...]
Recent human data have demonstrated that the SEEKING brain circuitry, as predicted, is involved in the emergence of a characteristic appetitive affective state, which may be described as “enthusiastic positive excitement” or “euphoria” (Drevets et al., 2001; Volkow and Swanson, 2003) and that do not resemble any kind of sensory pleasure (Heath, 1996; Panksepp et al., 1985).
Last edited by Petter; 07-05-2023 at 08:34 AM.
https://pubmed.ncbi.nlm.nih.gov/3038140/
Dorsomedial diencephalic involvement in the juvenile play of rats
Lesions of either the dorsomedial thalamus (DMT) or the parafascicular region of the thalamus (PFA) reduced rough-and-tumble social play in juvenile rats, as measured by frequency of pinning. Pinning was reduced by 33% in pups with DMT lesions and by 73% in pups with PFA lesions. Although PFA lesions had minimal effects on average pin durations, DMT pups had pins that were, on average, 105% longer than those of controls. Lesions of the PFA, but not DMT, also reduced play solicitation behaviors. Pups with PFA lesions were also insensitive to the play modulating effects of both naloxone and morphine. DMT pups were sensitive to the facilitatory effects of morphine, but naloxone was without effect in these animals. Control studies designed to evaluate general behavioral competence showed that the observed lesion effects were relatively specific to play.
https://www.huffpost.com/entry/depre...g-sy_b_3616967
In fact, for Panksepp, this SEEKING System is implicated in everything from our constant meaning-making (searching the environment for significant connections) to, in its excessive form, addictions. "Check out a cocaine addict cruising for a new fix," Panksepp observed. Or someone addicted to the internet, going from one Google search to another. Dopamine is firing, keeping the human being in a constant state of alert expectation.
Typically it is not the reward that makes us feel euphoric, but the search itself.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181986/
But what systems are they? Here, arguments for the critical importance of brain systems that integrate the distress and despair of separation-distress (overactivity of basic PANIC/GRIEF networks) and the diminished arousal of SEEKING networks that constitute dysphoria will be presented.
[...]
Excessive arousal of SEEKING urges may contribute substantially to mania and psychostimulant addictions, leading to excessive elation/euphoria, arising from excessive appetitive dopamine SEEKING urges, which can promote unwise life choices.
[...]
Human and animal sadness and animal separation-distress/GRIEF systems. Animal data comes from mapping of separation distress circuits with localized electrical stimulation in guinea pigs and human data from PET imaging of affective states by Damasio's group. AC, anterior cingulate; VS, ventral striatum; dPOA, dorsal preoptic area; BN, bed nucleus of the stria terminalis; DMT, dorsomedial thalamus; PAG, periaqueductal gray.
basic emotions Jaak Panksepp 4.jpg
Last edited by Petter; 07-05-2023 at 08:12 AM.
https://en.wikipedia.org/wiki/Euphoria
"Playing can induce an intense state of happiness and contentment, like this girl playing in the snow."
But is it euphoria?
happiness or euphoria.jpg
excitement, euphoria 1 <--> pleasure-seeking, goal-directed behavior
enjoyment, euphoria 2 <--> jocularity, grandiosity
neurotransmitters 3 b.jpg
https://academic.oup.com/brain/artic...10/2121/314497
Neural correlates of laughter and humour
Although laughter and humour have been constituents of humanity for thousands if not millions of years, their systematic study has begun only recently. Investigations into their neurological correlates remain fragmentary and the following review is a first attempt to collate and evaluate these studies, most of which have been published over the last two decades. By employing the classical methods of neurology, brain regions associated with symptomatic (pathological) laughter have been determined and catalogued under other diagnostic signs and symptoms of such conditions as epilepsy, strokes and circumspect brain lesions. These observations have been complemented by newer studies using modern non‐invasive imaging methods. To summarize the results of many studies, the expression of laughter seems to depend on two partially independent neuronal pathways. The first of these, an ‘involuntary’ or ‘emotionally driven’ system, involves the amygdala, thalamic/hypo‐ and subthalamic areas and the dorsal/tegmental brainstem. The second, ‘voluntary’ system originates in the premotor/frontal opercular areas and leads through the motor cortex and pyramidal tract to the ventral brainstem. These systems and the laughter response appear to be coordinated by a laughter‐coordinating centre in the dorsal upper pons. Analyses of the cerebral correlates of humour have been impeded by a lack of consensus among psychologists on exactly what humour is, and of what essential components it consists. Within the past two decades, however, sufficient agreement has been reached that theory‐based hypotheses could be formulated and tested with various non‐invasive methods. For the perception of humour (and depending on the type of humour involved, its mode of transmission, etc.) the right frontal cortex, the medial ventral prefrontal cortex, the right and left posterior (middle and inferior) temporal regions and possibly the cerebellum seem to be involved to varying degrees. An attempt has been made to be as thorough as possible in documenting the foundations upon which these burgeoning areas of research have been based up to the present time.
https://pubmed.ncbi.nlm.nih.gov/27085503/
Structural and functional associations of the rostral anterior cingulate cortex with subjective happiness
Happiness is one of the most fundamental human goals, which has led researchers to examine the source of individual happiness. Happiness has usually been discussed regarding two aspects (a temporary positive emotion and a trait-like long-term sense of being happy) that are interrelated; for example, individuals with a high level of trait-like subjective happiness tend to rate events as more pleasant. In this study, we hypothesized that the interaction between the two aspects of happiness could be explained by the interaction between structure and function in certain brain regions. Thus, we first assessed the association between gray matter density (GMD) of healthy participants and trait-like subjective happiness using voxel-based morphometry (VBM). Further, to assess the association between the GMD and brain function, we conducted functional magnetic resonance imaging (MRI) using the task of positive emotion induction (imagination of several emotional life events). VBM indicated that the subjective happiness was positively correlated with the GMD of the rostral anterior cingulate cortex (rACC). Functional MRI demonstrated that experimentally induced temporal happy feelings were positively correlated with subjective happiness level and rACC activity. The rACC response to positive events was also positively correlated with its GMD. These results provide convergent structural and functional evidence that the rACC is related to happiness and suggest that the interaction between structure and function in the rACC may explain the trait-state interaction in happiness.
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.
Last edited by Petter; 07-06-2023 at 03:22 PM.
CARE ---> relaxedness ---> PLAY (happiness) ---> laughing
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