Basic Emotions
https://www.the16types.info/vbulleti.../51596-Model-D (page 14-17)
G)
happiness: serotonin 2 and noradrenaline (high)
sadness: serotonin 2 and noradrenaline (low)
calmness, contentment: serotonin 1 and noradrenaline (low)
stress, nervousness (---> anger and fear): serotonin 1 and noradrenaline (high)
excitement, interest (including surprise): dopamine and noradrenaline (high)
boredom, fatigue: dopamine and noradrenaline (low)
https://www.simonsfoundation.org/201...h-of-a-reward/
"The neurotransmitter famously provides the thrill we get from a surprise, a phenomenon known as reward prediction error. But growing evidence suggests the chemical also tracks movement, novelty and other neurobiological factors."
https://journals.sagepub.com/doi/pdf...69881117725915
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5606297/ (Serotonin and brain function: a tale of two receptors)
"Previous attempts to identify a unified theory of brain serotonin function have largely failed to achieve consensus. In this present synthesis, we integrate previous perspectives with new and older data to create a novel bipartite model centred on the view that serotonin neurotransmission enhances two distinct adaptive responses to adversity, mediated in large part by its two most prevalent and researched brain receptors: the 5-HT1A and 5-HT2A receptors. We propose that passive coping (i.e. tolerating a source of stress) is mediated by postsynaptic 5-HT1AR signalling and characterised by stress moderation. Conversely, we argue that active coping (i.e. actively addressing a source of stress) is mediated by 5-HT2AR signalling and characterised by enhanced plasticity (defined as capacity for change). We propose that 5-HT1AR-mediated stress moderation may be the brain’s default response to adversity but that an improved ability to change one’s situation and/or relationship to it via 5-HT2AR-mediated plasticity may also be important – and increasingly so as the level of adversity reaches a critical point. We propose that the 5-HT1AR pathway is enhanced by conventional 5-HT reuptake blocking antidepressants such as the selective serotonin reuptake inhibitors (SSRIs), whereas the 5-HT2AR pathway is enhanced by 5-HT2AR-agonist psychedelics. This bipartite model purports to explain how different drugs (SSRIs and psychedelics) that modulate the serotonergic system in different ways, can achieve complementary adaptive and potentially therapeutic outcomes."
"This said, it is intriguing to consider the possibility that a ‘loosened mind’, whether subsequent to enhanced 5-HT2AR signalling or not, may be a non-negligible component of the neurobiology of positive mood itself (Ashby et al., 1999). Blocking the 5-HT2AR has been found to significantly attenuate the positive mood effects of three different classic psychedelics (Kometer et al., 2012; Preller, 2016; Valle et al., 2016) and MDMA (van Wel et al., 2012), and it is intriguing to consider whether 5-HT2AR-mediated plasticity may be an underappreciated component of the antidepressant action of SSRIs (Chamberlain et al., 2006; Petit et al., 2014; Qesseveur et al., 2016). Several studies have demonstrated a relationship between positive mood and creative thinking (De Dreu et al., 2008; Hirt et al., 2008), with the elation, flight of ideas and general hyper-creativity of manic states being relevant in this context (Jamison, 1994).
‘The secret to happiness is freedom’. (Thucydides c. 450BC)
It is presumed that the brain (like the mind) functions in a freer, less constrained manner during creative states, as during positive mood..."
serotonin.png
https://www.frontiersin.org/articles...015.00253/full
"Risk-taking was modulated by emotional context: fear and anger influenced risk-taking specifically in the gain frame and had opposite effects. Fear increased risk-averse choices, whereas anger decreased risk-averse choices, leading to a suppression of the framing effect. These results confirm that emotions play a key role in framing susceptibility."
https://www.nature.com/articles/s41598-018-28863-3
"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."
"Pertaining to the brain activation patterns underlying anger, the majority of neuroimaging studies have investigated this emotion indirectly by showing angry faces, or by using recall, imagery, or rumination of anger-eliciting situations. The results of these studies are very divergent in their findings. Whereas some findings point to an involvement of the orbitofrontal cortex, other results suggest reduced activations in the orbitofrontal cortex and somatosensory cortex as well as increased activations in the anterior cingulate cortex (ACC) and insula. Still other studies found an association of the temporal poles, or the dorsal anterior cingulate cortex with anger."
https://www.healthline.com/health/st...mygdala-hijack
"The amygdala activates this fight-or-flight response without any initiative from you. When that part of your brain senses danger, it signals your brain to pump stress hormones, preparing your body to either fight for survival or to flee to safety."
https://www.psychologytoday.com/us/b...od-bad-or-both
"Here, in brief, is how the survival-oriented acute stress response operates. Accurately or not, if you assess the immediately menacing force as something you potentially have the power to defeat, you go into fight mode. In such instances, the hormones released by your sympathetic nervous system—especially adrenaline—prime you to do battle and, hopefully, triumph over the hostile entity.
Conversely, if you view the antagonistic force as too powerful to overcome, your impulse is to outrun it (and the faster the better). And this, of course, is the flight response, also linked to the instantaneous ramping up of your emergency biochemical supplies—so that, ideally, you can escape from this adversarial power (whether it be human, animal, or some calamity of nature).
Where, in what you perceive as a dire threat, is the totally disabling freeze response? By default, this reaction refers to a situation in which you’ve concluded (in a matter of seconds—if not milliseconds) that you can neither defeat the frighteningly dangerous opponent confronting you nor safely bolt from it. And ironically, this self-paralyzing response can, in the moment, be just as adaptive as either valiantly fighting the enemy or, more cautiously, fleeing from it."
anger and fear.jpg
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3858647/
"Novelty and surprise play significant roles in animal behavior and in attempts to understand the neural mechanisms underlying it. They also play important roles in technology, where detecting observations that are novel or surprising is central to many applications, such as medical diagnosis, text processing, surveillance, and security. Theories of motivation, particularly of intrinsic motivation, place novelty and surprise among the primary factors that arouse interest, motivate exploratory or avoidance behavior, and drive learning. In many of these studies, novelty and surprise are not distinguished from one another: the words are used more-or-less interchangeably. However, while undeniably closely related, novelty and surprise are very different. The purpose of this article is first to highlight the differences between novelty and surprise and to discuss how they are related by presenting an extensive review of mathematical and computational proposals related to them, and then to explore the implications of this for understanding behavioral and neuroscience data. We argue that opportunities for improved understanding of behavior and its neural basis are likely being missed by failing to distinguish between novelty and surprise."
https://www.sciencedaily.com/release...1127161446.htm
"A Columbia University study in fruit flies has identified serotonin as a chemical that triggers the body's startle response, the automatic deer-in-the-headlights reflex that freezes the body momentarily in response to a potential threat."
https://www.psychologytoday.com/us/b...us-wonder-twin
"Norepinephrine (also called noradrenaline) is ‘adrenaline for your brain’. Just as adrenaline revs up your body, norepinephrine revs up your brain."
Agape is that you?
https://www.huffpost.com/entry/hacki...py-c_b_6007660
"Serotonin flows when you feel significant or important. Loneliness and depression appears when serotonin is absent. It's perhaps one reason why people fall into gang and criminal activity -- the culture brings experiences that facilitate serotonin release. Unhealthy attention-seeking behavior can also be a cry for what serotonin brings. Princeton neuroscientist Barry Jacobs explains that most antidepressants focus on the production of serotonin.
Reflecting on past significant achievements allows the brain to re-live the experience. Our brain has trouble telling the difference between what's real and imagined, so it produces serotonin in both cases. It's another reason why gratitude practices are popular. They remind us that we are valued and have much to value in life. If you need a serotonin boost during a stressful day, take a few moments to reflect on a past achievements and victories."
Oooh basic emotions, like maybe Paul Ekman and micro expressions and such!
Nope...nvm, it's neurochemistry. *Exits*
https://onlinelibrary.wiley.com/doi/...1111/jnc.15607
Happiness could be a self-conscious emotion (not a basic emotion) and it could be the same thing as pride.
https://time.com/4254089/science-crying/
"Crying signals to yourself and other people that there’s some important problem that is at least temporarily beyond your ability to cope"
stress and nervousness (---> tension): a threat/a problem <--> serotonin 1
anger and fear: the fight-or-flight response <--> noradrenaline (high)
happiness/pride (satisfaction with achievement): actively addressing a source of stress <--> serotonin 2 ... a self-conscious emotion
contempt: someone is causing a threat (blame) ... a self-conscious emotion
excitement and interest (including surprise): motivation <--> dopamine
disgust <--> serotonin 3 ... a basic emotion?
work ---> pleasure
the goal is always pleasure (dopamine)
work causes stress (serotonin)
To me, work causes pleasure and doing nothing causes stress.Originally Posted by Petter
https://theconversation.com/the-evol...njoyment-57750
"While laughter has been linked to higher pain tolerance and the signalling of social status, its principal function appears to be creating and deepening social bonds."
calmness, contentment <--> serotonin (high)
tension, nervousness (or fear) <--> serotonin (low)
interest (novelty and surprise) <--> noradrenaline (high)
boredom <--> noradrenaline (low)
excitement <--> dopamine (high)
dispiritedness <--> dopamine (low)
fascination = excitement + interest
terror = tension + interest (high)
anger = tension + excitement
rage = tension + excitement + interest (high)
happiness = calmness + excitement + interest
sadness = tension + dispiritedness + boredom
... or attractionfascination = excitement + interest
https://www.tandfonline.com/doi/abs/...nalCode=pcem20
"Tornochuk and Ellis argue that DISGUST should be considered a basic emotional system, on a par with the other basic emotional systems such as SEEKING, FEAR, RAGE, LUST, CARE, PANIC and PLAY, which constitute the groundwork for a cross-species emotion neuroscience with immediate implications for understanding emotional imbalances that characterise psychiatric disorders. Disgust is clearly a basic sensory/interoceptive affect (Rozin & Fallon, 1987), and a socially constructed moral emotion (Haidt, 2003a, b), but perhaps it is a category error to classify disgust as a basic emotion. It is more akin to a sensory affect. If we consider sensory disgust to be a basic emotional systems, then why not include hunger, thirst, fatigue and many other affective states of the body as emotions?"
https://en.wikipedia.org/wiki/Seroto...nervous_system
"If irritants are present in the food, the enterochromaffin cells release more serotonin to make the gut move faster, i.e., to cause diarrhea, so the gut is emptied of the noxious substance. If serotonin is released in the blood faster than the platelets can absorb it, the level of free serotonin in the blood is increased. This activates 5-HT3 receptors in the chemoreceptor trigger zone that stimulate vomiting."
(outside the nervous system)
https://www.cam.ac.uk/research/news/...ponse-to-anger
"The research revealed that low brain serotonin made communications between specific brain regions of the emotional limbic system of the brain (a structure called the amygdala) and the frontal lobes weaker compared to those present under normal levels of serotonin. The findings suggest that when serotonin levels are low, it may be more difficult for the prefrontal cortex to control emotional responses to anger that are generated within the amygdala."
https://www.frontiersin.org/articles...016.00024/full
"The amygdala is a key player in the processing of fear. This brain area is prominently modulated by the neurotransmitter serotonin (5-hydroxytryptamine, 5-HT)."
"Two aspects suggest that 5-HT may influence emotional processing, at least in part, via modulation of amygdala function. First, drugs that block the re-uptake of 5-HT (e.g., selective serotonin reuptake inhibitors, SSRIs), the first-line treatment for depression and anxiety (Preskorn et al., 2004), affect amygdala activation to emotional stimuli (Bigos et al., 2008; Murphy et al., 2009; Godlewska et al., 2012). Second, genetic variations in the 5-HT transporter (5-HTT) influence amygdala activation to aversive stimuli, as well as expression of anxiety-related personality traits and risk for affective disorders (Lesch et al., 1996; Hariri et al., 2002)."
https://en.wikipedia.org/wiki/Locus_coeruleus
"The LC's role in cognitive function in relation to stress is complex and multi-modal. Norepinephrine released from the LC can act on α2 receptors to increase working memory, or an excess of NE may decrease working memory by binding to the lower-affinity α1 receptors."
https://www.smh.com.au/national/dopa...12-gdicc5.html
"Dopamine, on the other hand, makes us excitable. When we lose our temper, it is dopamine, and adrenaline, that overwhelms us and triggers the fight-or-flight response that used to save us from sabre-tooth tigers and the like."
https://www.nature.com/articles/s41467-021-27092-z
"dopamine system hyperactivity is associated with elevated aggression"
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2612120/
"Specifically, serotonin hypofunction may represent a biochemical trait that predisposes individuals to impulsive aggression, with dopamine hyperfunction contributing in an additive fashion to the serotonergic deficit."
https://www.psychologytoday.com/us/b...addicted-anger
"What happens is that anger can lead to similar “rushes” as thrill-seeking activities where danger triggers dopamine reward receptors in the brain, or like other forms of addiction such as gambling, extreme sports, or even drugs like cocaine and methamphetamines. Anger can become its own reward, but like other addictions, the final consequences are dangerous and real, and people follow impulses in the moment without regard to the big picture."
https://www.uu.se/en/news/article/?i...rtikel&lang=en
"This discovery is a major leap forward when it comes to identifying changes in the brain’s chemical messengers in people who suffer from anxiety. Earlier research has shown that nerve activity in the amygdala is higher in people with social phobia and thus that the brain’s fear centre is over-sensitive. The new findings indicate that a surplus of serotonin is part of the underlying reason."
https://www.jneurosci.org/content/40/24/4739
"The causal relationship between amygdala serotonin levels and an animal's sensitivity to threat was confirmed via direct amygdala infusions of a selective serotonin reuptake inhibitor (SSRI), citalopram. Both anxiety-like behaviors, and conditioned threat-induced responses were reduced by the blockade of serotonin reuptake in the amygdala."
https://www.reuters.com/article/us-d...79946320080605
"Low levels of key brain chemical sparks anger"
"Serotonin, the nerve-signaling chemical targeted by many antidepressants, appears to keep aggressive social responses in check, Molly Crockett, a psychologist at the University of Cambridge and colleagues reported in the journal Science.
The chemical’s precise role in impulse control has been controversial but this study is one of the first to actually show a causal link, Crockett said."
https://en.wikipedia.org/wiki/Reward...ing_and_liking
"The wanting component is thought to be controlled by dopaminergic pathways, whereas the liking component is thought to be controlled by opiate-benzodiazepine systems."
https://www.sciencedirect.com/scienc...91305797002773
"Numerous studies have demonstrated that activation of serotonin 5-HT1A or 5-HT1B receptor decreases aggression in male mammals."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4606977/
"The serotonin 2A (5-HT2A) receptor has been implicated in neural-processing of emotionally salient information. To elucidate its role in processing of fear and anger, healthy individuals were studied with functional MRI (fMRI) after 5-HT2A receptor blockade, while judging the gender of neutral, fearful and angry faces."
https://psychopharmacologyinstitute....tion-2064-4160
"The 5-HT has many roles in the brain but one of the most reliable behavioral effects of 5-HT is to regulate impulsivity and aggression. We know that if we reduce 5-HT in the brain by depleting the brain of the precursor tryptophan, so 5-HT level is full, we get increased impulsive and aggressive behaviors."
"Like impulsivity and aggression, anxiety can be negatively modulated. We can downregulate anxiety by stimulating the 5-HT1A receptor. So for instance, with the releasing drug MDMA, but more obviously in clinical practice with SSRI treatment over several weeks, we can increase serotonin, stimulate those postsynaptic 1A receptors in the stress-sensitive limbic regions and reduce anxiety. And it’s important to note that the 5-HT1A receptor here is an inhibitory receptor. It dampens down overactivity of the limbic system and therefore reduces anxiety."
"There is a much higher density of the 2A receptor in cortical regions compared with the 1A receptor. The 1A receptor has a particularly high expression in areas like the hippocampus that’s part of the limbic system."
"In contrast, cognitive flexibility is thought to be modulated by the 5-HT2A receptor. And there is evidence that stimulation of the 5-HT2A receptor with agonists such as LSD and psilocybin enhance cognitive flexibility and can improve creative thinking."
https://burgundyzine.com/5-ht2a-from...to-psychiatry/
"Interestingly, however, the International Journal of Neuropsychopharmacology study found 5-HT2A and 5-HT2C agonists (blocking/inhibiting those receptors) were successful in reducing compulsive behavior."
"There’s a lot of evidence to suggest 5-HT2A is tied to mental wellbeing."
https://pubmed.ncbi.nlm.nih.gov/29555857/
"The current results demonstrate that activity in areas of the "social brain" can be modulated via the 5-HT2AR..."
https://www.sciencedirect.com/scienc...24977X18302827
"The serotonergic neurotransmitter system has been suggested to play a substantial role in modulating the DMN."
https://pubmed.ncbi.nlm.nih.gov/24926868/
"The therapeutics of obsessive-compulsive disorder (OCD) involves the serotonergic system in the brain; the selective serotonin reuptake inhibitors (SSRIs) are the only class of drugs to be consistently effective for this disorder. Preclinical studies in the orbito-frontal cortex - a brain area known to be involved in mediation of OCD symptoms - show that sustained administration of SSRI for 2 months leads to enhanced 5-HT release. Initially, raised 5-HT levels, resulting from serotonin (5-HT) reuptake inhibition, over-activates the cell body 5-HT1A autoreceptor, which has an inhibitory effect on the neuronal firing rate."
https://www.sciencedirect.com/topics...-hydroxylase-2
"Effect of central 5-HT deficiency on rodent behavior." (Figure 35.1)
https://www.biologicalpsychiatryjour...332-9/fulltext
"In summary, some evidence indicates that impulsive aggression is related to high brainstem 5-HTT, high global 5-HT4 and striatal 5-HT1B receptor binding, and low global MAOA levels. Collectively, these findings support an inverse association between serotonin and impulsive aggression, as considered in the following.
A high receptor binding potential as measured with PET could reflect an increased receptor density as a trait marker of impulsive aggression, or it could be explained by a reduction in interstitial serotonin. Low serotonin levels reduce the occupancy of the receptors, which may induce a compensatory upregulation of the receptor if the reduction is (semi-)chronic (46). In either case, the observed increases in 5-HT1B and 5-HT4 receptor binding support the serotonin deficiency theory of impulsive aggression, further supported by low brain levels of MAOA, which may be interpreted as an index of low serotonin turnover. A high brainstem 5-HTT presumably leads to more efficient reuptake of serotonin and thus lower brainstem interstitial serotonin. This leads to less firing from the 5-HT1A autoreceptors, resulting in higher serotonin production and subsequently higher postsynaptic release of serotonin, unless, of course, brainstem 5-HTT density is increased in response to chronically low brainstem serotonin levels."
https://royalsocietypublishing.org/d...rstb.2012.0039 (Targeting brain serotonin synthesis ... long-term outcomes related to negative emotionality, aggression and antisocial behaviour)
serotonin 4.jpg
Last edited by Petter; 07-18-2022 at 09:00 AM.
anger <--> serotonin (low)calmness, contentment <--> serotonin (high medium or balanced)
tension, nervousness (or fear) <--> serotonin (low high)
serotonin 2 <--> problem-solving (which is indirectly related to a threat)
sadness: pessimism ---> serotonin 2 (low) ---> dopamine (low) and noradrenaline (low)
https://news.mit.edu/2022/noradrenal...-surprise-0601https://www.simonsfoundation.org/201...h-of-a-reward/
"The neurotransmitter famously provides the thrill we get from a surprise, a phenomenon known as reward prediction error. But growing evidence suggests the chemical also tracks movement, novelty and other neurobiological factors."
"What this work shows is that the locus coeruleus encodes unexpected events, and paying attention to those surprising events is crucial for the brain to take stock of its environment"
https://www.sciencedaily.com/release...0107121453.htm
"How can we shift from a state of inattentiveness to one of highest attention? The locus coeruleus, literally the "blue spot," is a tiny cluster of cells at the base of the brain. As the main source of the neurotransmitter noradrenaline, it helps us control our attentional focus. Synthesizing evidence from animal and human studies, scientists at the Max Planck Institute for Human Development and the University of Southern California have now developed a novel framework describing the way the blue spot regulates our brain's sensitivity to relevant information in situations requiring attention. Their findings have been published in an opinion article in the journal Trends in Cognitive Sciences."
https://www.frontiersin.org/articles...016.00571/full
"According to our model of the regulation of appetitive-searching vs. distress-avoiding behaviors, the motivation to display these essential conducts is regulated by two parallel cortico-striato-thalamo-cortical, re-entry circuits, including the core and the shell parts of the nucleus accumbens, respectively. An entire series of basal ganglia, running from the caudate nucleus on one side, to the centromedial amygdala on the other side, controls the intensity of these reward-seeking and misery-fleeing behaviors by stimulating the activity of the (pre)frontal and limbic cortices. Hyperactive motivation to display behavior that potentially results in reward induces feelings of hankering (relief leads to pleasure). Hyperactive motivation to exhibit behavior related to avoidance of misery results in dysphoria (relief leads to happiness). These two systems collaborate in a reciprocal fashion. In clinical depression, a mismatch exists between the activities of these two circuits: the balance is shifted to the misery-avoiding side. Five theories have been developed to explain the mechanism of depressive mood disorders, including the monoamine, biorhythm, neuro-endocrine, neuro-immune, and kindling/neuroplasticity theories. This paper describes these theories in relationship to the model (described above) of the regulation of reward-seeking vs. misery-avoiding behaviors. Chronic stress that leads to structural changes may induce the mismatch between the two systems. This mismatch leads to lack of pleasure, low energy, and indecisiveness, on one hand, and dysphoria, continuous worrying, and negative expectations on the other hand. The neuroplastic effects of monoamines, cortisol, and cytokines may mediate the induction of these structural alterations. Long-term exposure to stressful situations (particularly experienced during childhood) may lead to increased susceptibility for developing this condition. This hypothesis opens up the possibility of treating depression with psychotherapy. Genetic and other biological factors (toxic, infectious, or traumatic) may increase sensitivity to the induction of relevant neuroplastic changes. Reversal or compensation of these neuroplastic adjustments may explain the effects of biological therapies in treating depression."
https://www.ncbi.nlm.nih.gov/books/NBK10854/
"In contrast to the relatively restricted responses generated by norepinephrine and acetylcholine released by sympathetic and parasympathetic ganglion cells, respectively, neurons of the enteric nervous system achieve an enormous diversity of target effects by virtue of many different neurotransmitters..."
https://link.springer.com/chapter/10...-7091-8341-0_4
"Noradrenaline and adrenaline inhibit acetylcholine release due to nerve activity, through α-adrenoceptors. The inhibition of acetylcholine release by the adrenergic transmitters is, in fact, a rather economical way for the adrenergic (orthosympathetic) nervous system to counteract the parasympathetic nervous system. It is shown that there is a permanent adrenergic control of acetylcholine output."
https://journals.plos.org/ploscompbi...l.pcbi.1009435
"How the brain decides which experiences to encode to memory and which to discard is a fundamental question in neuroscience. The neuromodulators acetylcholine and noradrenaline are believed to separately play a central role in determining what is encoded but the mechanisms by which they act are mostly unknown and there have been no direct comparisons made between these two critical neuromodulators."
neurotransmitters 2.jpg
neurotransmitters depression.png
Last edited by Petter; 07-05-2022 at 07:51 AM.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3260787/
"The goal of this paper is to consider anger from a cognitive neuroscience perspective. Five main claims are made: First, reactive aggression is the ultimate behavioral expression of anger and thus we can begin to understand anger by understanding reactive aggression. Second, neural systems implicated in reactive aggression (amygdala, hypothalamus and periaqueductal gray; the basic threat system) are critically implicated in anger. Factors such as exposure to extreme threat that increase the responsiveness of these systems, should be (and are in the context of Post Traumatic Stress Disorder), associated with increased anger. Third, regions of frontal cortex implicated in regulating the basic threat system, when dysfunctional (e.g., in the context of lesions) should be associated with increased anger. Fourth, frustration occurs when an individual continues to do an action in the expectation of a reward but does not actually receive that reward, and is associated with anger. Individuals who show impairment in the ability to alter behavioral responding when actions no longer receive their expected rewards should be (and are in the context of psychopathy) associated with increased anger. Fifth, someone not doing what another person wants them to do (particularly if this thwarts the person’s goal) is frustrating and consequently anger inducing. The response to such a frustrating social event relies on the neural architecture implicated in changing behavioral responses in non-social frustrating situations."
https://www.science.org/doi/10.1126/science.1082244 (Effects of Gaze on Amygdala Sensitivity to Anger and Fear Faces)
Last edited by Petter; 07-05-2022 at 07:39 AM.
https://www.endocrineweb.com/endocrinology/cortisol
"Cortisol gets a bad rap. As the body’s primary stress hormone, cortisol surges when we perceive danger, and causes all the symptoms we associate with “fight or flight”—increased blood pressure and heart rate, muscle tension, and the digestive system slamming to a halt, resulting in nausea, vomiting, and diarrhea."
https://www.cambridge.org/core/journ...B5CB9AEDF33552
"The fact that patients with major depression exhibit decreased brain serotonin (5-hydroxytryptamine, 5-HT) function and elevated cortisol secretion has reached the status of textbook truism. More recent formulations have suggested that elevated cortisol levels, probably caused by stressful life events, may themselves lower brain 5-HT function and this in turn leads to the manifestation of the depressive state (see Reference DinanDinan, 1994). This elegant proposal neatly ties abnormalities of cortisol secretion and 5-HT function into a causal chain in which cortisol is the key biological mediator through which life stress lowers brain 5-HT function, thereby causing depression in vulnerable individuals."
"The findings of Strickland et al (2002, this issue) suggest that some patients with depression (for example, those reporting recent severe life events) do hypersecrete cortisol. However, elevated cortisol levels after life events are not necessarily associated with the development of depressive disorder. Furthermore, the majority of patients with moderate depression in the community probably do not hypersecrete cortisol. It seems more likely that people with depression in the community exhibit abnormal brain 5-HT function, although the cause of this abnormality requires further study."
serotonin cortisol 2.jpg
serotonin cortisol 3.jpg
Last edited by Petter; 07-11-2022 at 03:42 PM.
a threat (stress) <--> serotonin 1, cortisol, noradrenaline, adrenaline
anger
fear
distress
a problem (an indirect threat) <--> serotonin 2
frustration
concern/worry
sadness
Relaxedness, calmness and relief are not positive emotions. Instead, they describe an absence of negative emotions. This means that positive/negative valence is an incorrect dimension of emotions.
basic emotions future and past.png
two dimensions of emotion.png
Emotion as a carousel of symphony ranked categories to rationalize and understand our sigils and axioms of the candle of love and honor makes us free to imagine and embody timeless themes and messages from the pool of ideals to anime us as the characters with our emotions and divine expressions infinitely.
Chinese Fortune Cookie ~ A fair face may fade, but a beautiful soul lasts forever. Lucky Numbers - 53, 10, 29, 14, 1, 21
Mr. Mime = Mastermind
Marius Florin aka LeoSuperCluster as Raging Bolt the Raikou number 1021 and SolitaryWalker brought glory to the years of Silver and forged Pichu, wisdom of force and flair to exhibit dinosaur questing pointers electrocuting cinema and blueprints of emporiums to undertow flows jungle tossing galaxy spanning shivers of essence gems and portals of roads to destruction and arboretums folding castles and swordsmanship of dreams and counters to pleasant vibrations and holy water sprouting evanescent stars and puzzles of grades to saffron climax
https://www.the16types.info/vbulleti...k-2024-edition
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2801060/ (Dopamine Enhances Expectation of Pleasure in Humans)
"Human action is strongly influenced by expectations of pleasure. Making decisions, ranging from which products to buy to which job offer to accept, requires an estimation of how good (or bad) the likely outcomes will make us feel. Yet, little is known about the biological basis of subjective estimations of future hedonic reactions. Here, we show that administration of a drug that enhances dopaminergic function (dihydroxy-L-phenylalanine; L-DOPA) during the imaginative construction of positive future life events subsequently enhances estimates of the hedonic pleasure to be derived from these same events. These findings provide the first direct evidence for the role of dopamine in the modulation of subjective hedonic expectations in humans."
https://www.intoactionrecovery.com/h...-our-behavior/
"Excitatory neurotransmitters encourage a cell to take action."
"Inhibitory neurotransmitters decrease the chances of a cell taking any type of action, leading to a relaxation-like effect on the body."
"Dopamine is an excitatory neurotransmitter. Dopamine communicates with brain cells and encourages them to act in a pleasurable, excitable, euphoric way. The excitatory nature of dopamine is also one of the reasons why the chemical messenger motivates us. By encouraging our brain cells to take certain actions, dopamine influences our behavior. But dopamine differs from most neurotransmitters. Even though dopamine is an excitatory neurotransmitter, the chemical messenger can encourage or prevent action depending on the receptors present."
https://www.medicalnewstoday.com/articles/326090#fa-qs
Do dopamine and serotonin make a person happy?
People often call dopamine and serotonin the “happy hormones,” because they promote mental well-being.
Dopamine, also known as the “feel-good” hormone, is associated with the brain’s reward system and produces pleasant sensations.
Serotonin can help increase happiness by alleviating depression and anxiety.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4899514/ (Noradrenaline effects on social behaviour, intergroup relations, and moral decisions)
"There is much evidence suggesting an interaction between NA and oxytocin, also with regards to regulating social behaviour. For example, Salmina et al. (2010) described evidence suggesting that oxytocin release was regulated by NA in the hypothalamic-neurophysical system, specifically including the supraoptic nucleus and the paraventricular nucleus (PVN). The authors argued that NA activates presynaptic glutamate interneurons closely located around PVN and therewith indirectly causes oxytocin release."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4449495/
"... neurotransmitters (e.g. dopamine, serotonin, norepinefrine and endorphin) play a role in control of happiness. A few studies pointed to the role of cortisol and adrenaline (adrenal gland) and oxitocin (pituitary gland) in controlling happiness."
https://www.apa.org/monitor/feb08/oxytocin
"New studies are adding to a body of literature that shows oxytocin plays a key role in maternal bonding and social affiliation-what Taylor has labeled the "tend and befriend" response, as opposed to the "fight or flight" response. In line with years of animal research linking oxytocin to mothers' ability to care for their infants, a study in the November Psychological Science (Vol. 18, No. 11, pages 965-970), demonstrates this association for the first time in people."
https://www.psycom.net/oxytocin
“I would argue the phrase ‘the cuddle hormone’ is a bit of a misnomer,” Brown says. While it’s true that oxytocin enhances bonding under certain circumstances, it may also lead to jealousy, suspicion, and the formation of “in” groups and “out” groups. “It seems the effect of oxytocin depends on the situation. So, when someone is in the presence of a person who is not part of their ‘tribe’ if you will, it can actually increase negative feelings toward members of the ‘out’ group. It’s not as straightforward of an explanation as we used to think,” Brown says.
https://www.medicalnewstoday.com/art...fits-of-crying
"As well as helping people self-soothe, crying can help people get support from others around them.
As this 2016 study explains, crying is primarily an attachment behavior, as it rallies support from the people around us. This is known as an interpersonal or social benefit."
"Crying may help lift people’s spirits and make them feel better. As well as relieving pain, oxytocin and endorphins can help improve mood."
https://www.backinline.com.au/power-...-nerve-system/
"Laughter can create instant bonds between individuals. The release of oxytocin occurs while laughing. Often called the empathy hormone, oxytocin helps bond individuals and collectives."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6713138/
"Complicated grief (CG) is a debilitating syndrome characterized by persisting and intense distress and impairment after the death of a loved one. The biological mechanisms associated with this syndrome remain unclear but may involve neurobiological pathways implicated in the stress response and attachment systems. The neuropeptide oxytocin has been implicated in attachment and social behaviour, and loss of social bonds has been associated with disruptions in oxytocin signalling."
neurotransmitters 3.png
Last edited by Petter; 07-17-2022 at 11:25 AM.
depression <--> a threat (stress)
sadness <--> social interaction
(?)
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