Basic Emotions

[Petter]

https://www.journals.uchicago.edu/doi/10.1086/498281

A number of recent hypotheses have attempted to explain the ultimate evolutionary origins of laughter and humor. However, most of these have lacked breadth in their evolutionary frameworks while neglecting the empirical existence of two distinct types of laughter—Duchenne and non‐Duchenne—and the implications of this distinction for the evolution of laughter as a signal. Most of these hypotheses have also been proposed in relative isolation of each other and remain disjointed from the relevant empirical literature. Here we attempt to remedy these shortcomings through a synthesis of previous laughter and humor research followed by (i) a reevaluation of this research in light of theory and data from several relevant disciplines, and (ii) the proposal of a synthetic evolutionary framework that takes into account phylogeny and history as well as proximate mechanisms and adaptive significance. We consider laughter to have been a preadaptation that was gradually elaborated and co‐opted through both biological and cultural evolution. We hypothesize that Duchenne laughter became fully ritualized in early hominids between 4 and 2 mya as a medium for playful emotional contagion. This mechanism would have coupled the emotions of small hominid groups and promoted resource‐building social play during the fleeting periods of safety and satiation that characterized early bipedal life. We further postulate that a generalized class of nonserious social incongruity would have been a reliable indicator of such safe times and thereby came to be a potent distal elicitor of laughter and playful emotion. This class of stimuli had its origins in primate social play and was the foundation for formal human humor. Within this framework, Duchenne laughter and protohumor were well established in the hominid biobehavioral repertoire when more cognitively sophisticated traits evolved in the hominid line between 2 mya and the present. The prior existence of laughter and humor allowed them to be co‐opted for numerous novel functions, and it is from this process that non‐Duchenne laughter and the “dark side” of laughter emerged. This perspective organizes the diversified forms and functions that characterize laughter and humor today and clarifies when and how laughter and humor evolved during the course of human evolution.

https://greatergood.berkeley.edu/art...hy_do_we_laugh

It may seem impossible to study humor; but scientists have found ways, mostly through large surveys and fMRI research. For example, to find out what makes a joke funny, a German researcher named Willibald Ruch asked subjects a series of questions about hundreds of jokes and cartoons. Based on their answers, he grouped humor preferences into three types: “incongruity-resolution,” which involves “violating one’s expectations in novel ways;” “nonsense humor,” “which is funny only because it makes no sense;” and “sexual humor,” which is offensive or taboo. Although not everyone finds the same type of humor funny, the common thread in these joke types is that they all involve dealing with surprise and resolving the ensuing cognitive dissonance.

“What elicits laughter isn’t the content of the joke but the way our brain works through the conflict the joke elicits,” writes Weems.

Take for example an old Groucho Marx joke: “One morning I shot an elephant in my pajamas. How he got in my pajamas, I don’t know.” Our brains will read the first sentence and be taken down a path imagining Grouch Marx on a safari in his pajamas, before we get the new image of the elephant actually inside his pajamas. That process of moving from one possible solution to the next involves a part of the brain called the anterior cingulate, or AC, which becomes more active when there are conflicting interpretations in the brain. The AC helps to quiet down the “louder” parts of the brain (associated with the expected response) to allow other quieter answers to emerge, and it’s particularly active during jokes. It helps us to figure out the novel solution, which, when resolved, gets incorporated into the brain and gives us that spike of dopamine. This is why we feel so good when we get a joke, and why jokes are not funny the second time around.

https://royalsocietypublishing.org/d...rstb.2021.0180

The web of laughter: frontal and limbic projections of the anterior cingulate cortex revealed by cortico-cortical evoked potential from sites eliciting laughter

According to an evolutionist approach, laughter is a multifaceted behaviour affecting social, emotional, motor and speech functions. Albeit previous studies have suggested that high-frequency electrical stimulation (HF-ES) of the pregenual anterior cingulate cortex (pACC) may induce bursts of laughter—suggesting a crucial contribution of this region to the cortical control of this behaviour—the complex nature of laughter implies that outward connections from the pACC may reach and affect a complex network of frontal and limbic regions. Here, we studied the effective connectivity of the pACC by analysing the cortico-cortical evoked potentials elicited by single-pulse electrical stimulation of pACC sites whose HF-ES elicited laughter in 12 patients. Once these regions were identified, we studied their clinical response to HF-ES, to reveal the specific functional target of pACC representation of laughter. Results reveal that the neural representation of laughter in the pACC interacts with several frontal and limbic regions, including cingulate, orbitofrontal, medial prefrontal and anterior insular regions—involved in interoception, emotion, social reward and motor behaviour. These results offer neuroscientific support to the evolutionist approach to laughter, providing a possible mechanistic explanation of the interplay between this behaviour and emotion regulation, speech production and social interactions.

[Petter]

https://royalsocietypublishing.org/d...rstb.2021.0180

Laughter represents a long-lasting and yet unsolved issue for neuroscientists. Traditionally, studies on the neural basis of laughter were primarily driven by clinical interests, laughter being a distinctive sign of different pathological conditions pertaining to brain lesions or epilepsy (see [1]). Such studies, focused on the pathological production of laughter, put in the spotlight the role of subcortical structures (e.g. hypothalamus, brainstem) in generating the motor pattern of laughter. This view was well-matched with mainstream psychological theories of laughter, which considered laughter as a peripheral motor output triggered by more interesting cognitive antecedents, such as humour appreciation, sense of superiority or cognitive incongruence [2].

Laughter, however, is not only a mere subcortical phenomenon. According to an emerging evolutionary social–functional account, laughter is a multifaceted social behaviour actively contributing to the reinforcement of ongoing interactions, affiliation and communicative intents [3–8]. It carries information on the behavioural intentions of the agent, and the identity and hierarchical position of the recipient. In addition, following a fortunate perspective initiated by James [9], the physical act of laughing, along with its interoceptive feedback, is conceived to be a quintessential element in the constitution of our perceived sense of happiness which, in turn, downregulates social anxiety and negative emotions [10–12]. Interpreting laughter as a genuine socio-emotional complex behaviour, rather than a peripheral consequence of humour appreciation, makes a case for its complex cerebral representation, moving beyond subcortical structures and potentially encompassing several regions of the social and emotional brain.

In the recent past, studies conducted in surgical patients demonstrated that laughter can be elicited from the pregenual anterior cingulate cortex (pACC) by using high-frequency electrical stimulation (HF-ES; [13–18]). In these studies, the motor act of laughter was often accompanied by a sense of merriment, along with autonomic responses and interoceptive sensations [14,15,17,18]. These findings suggest that the pregenual sector of the ACC (pACC) subfield contributing to laughter production (hereafter, pACC-L for brevity) may control both the motor and the emotional aspects of laughter, in line with William James' theory [19]. The emotional interpretation of pACC-L laughter is also substantiated by imaging studies—showing that this region is structurally and functionally associated with subjective happiness [20]—and tractography studies—showing descending connections from pACC-L to the ventral striatum [21], a key reward centre whose stimulation also elicits mirthful laughter [22,23]. However, whether pACC-L controls the motor act of laughter independently of the voluntary motor system is still unclear.

Concerning the link between pACC-L, emotional laughter and social cognition, we recently reported that the same pACC sector eliciting bursts of laughter when stimulated is also activated by the passive observation of others’ laughter [16]. This finding is in accord with the contribution of the anterior cingulate cortex to the facial mimicry of dynamic positive expressions [24], and leads to the hypothesis that the pACC-L hosts an emotional mirror system boosting laughter contagion [25–27].

[...]

Despite the predominant psychological theories of laughter regarding this behaviour as a peripheral motor output essentially pertaining to subcortical circuits, here we report that the outward connections of the pACC sector involved in the production of mirthful laughter reach a high number of cortical regions. Connected regions include the adjacent cingulate and medial prefrontal cortices, the OFC and the anterior insula, contributing to interoception, emotion, social reward and motor behaviour. Of note, the pACC-L effective connectivity spares both motor and premotor regions—confirming that the pACC-L controls emotional laughter independently from the voluntary motor system—and temporal regions encoding humour—supporting the independence of laughter from humour appreciation. These results offer neuroscientific support to the evolutionary socio-emotional theory of laughter, providing a possible mechanistic explanation of the interplay between this behaviour and emotion regulation, speech production and social interactions.

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https://i.imgur.com/alJDBFv.gif

[Petter]

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

[Petter]

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://edition.cnn.com/2021/07/01/h...ess/index.html

"Laughter is thought to have evolved as a form of social bonding in animals and as a way to express playful intention. Many mammals laugh when they are tickled and when they engage in physical play."

https://science.howstuffworks.com/li.../laughter2.htm

Provine is among only a few people who are studying laughter much as an animal behaviorist might study a dog's bark or a bird's song. He believes that laughter, like the bird's song, functions as a kind of social signal. Other studies have confirmed that theory by proving that people are 30 times more likely to laugh in social settings than when they are alone (and without pseudo-social stimuli like television). Even nitrous oxide, or laughing gas, loses much of its oomph when taken in solitude, according to German psychologist Willibald Ruch.

https://www.sciencedirect.com/scienc...0105112200120X

"Oxytocin promotes laughing and smiling"

https://science.howstuffworks.com/li.../laughter5.htm

Laughter is triggered when we find something humorous. There are three traditional theories about what we find humorous:

The incongruity theory suggests that humor arises when logic and familiarity are replaced by things that don't normally go together. Researcher Thomas Veatch says a joke becomes funny when we expect one outcome and another happens. When a joke begins, our minds and bodies are already anticipating what's going to happen and how it's going to end. That anticipation takes the form of logical thought intertwined with emotion and is influenced by our past experiences and our thought processes. When the joke goes in an unexpected direction, our thoughts and emotions suddenly have to switch gears. We now have new emotions, backing up a different line of thought. In other words, we experience two sets of incompatible thoughts and emotions simultaneously. We experience this incongruity between the different parts of the joke as humorous.

The superiority theory comes into play when we laugh at jokes that focus on someone else's mistakes, stupidity or misfortune. We feel superior to this person, experience a certain detachment from the situation and so are able to laugh at it.

The relief theory is the basis for a device movie-makers have used effectively for a long time. In action films or thrillers where tension is high, the director uses comic relief at just the right times. He builds up the tension or suspense as much as possible and then breaks it down slightly with a side comment, enabling the viewer to relieve himself of pent-up emotion, just so the movie can build it up again! Similarly, an actual story or situation creates tension within us. As we try to cope with two sets of emotions and thoughts, we need a release and laughter is the way of cleansing our system of the built-up tension and incongruity. (According to Dr. Lisa Rosenberg, humor, especially dark humor, can help workers cope with stressful situations. "The act of producing humor, of making a joke, gives us a mental break and increases our objectivity in the face of overwhelming stress," she says.)

https://web.archive.org/web/20190226...2c64ba35e3.pdf

[Petter]

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4534772/

Humour detection accuracy was associated with grey matter volume in a distributed network including temporo-parietal junctional and anterior superior temporal cortices, with predominantly left-sided correlates of processing humour in familiar scenarios and right-sided correlates of processing novel humour. The findings quantify deficits of core cognitive operations underpinning humour processing in frontotemporal lobar degenerations and suggest a candidate brain substrate in cortical hub regions processing incongruity and semantic associations.

[...]

Neuroanatomical correlates of humour cognition were assessed using voxel-based morphometry (VBM). Drawing on previous neuroimaging evidence to guide a region-of-interest analysis (Goel & Dolan, 2001; Mobbs et al., 2003; Moran et al., 2004; Neely et al., 2012; Wild et al., 2006), we hypothesised regional grey matter correlations of altered humour processing in a distributed brain network including temporo-parieto-occipital junction, anterior temporal lobe, ventromedial prefrontal and anterior cingulate cortex. Within this network, certain key ‘hubs’ have been identified. Cortical areas in the region of the temporo-parieto-occipital junction (especially in the left cerebral hemisphere) may mediate humour detection and analysis of potentially humorous (in particular, incongruous) stimuli, based on prior expectations and stored concepts (Coulson & Kutas, 2001; Franklin & Adams, 2011; Goel & Dolan, 2001; Gold & Buckner, 2002; Moran et al., 2004; Neely et al., 2012; Schurz, Aichhorn, Martin, & Perner, 2013; Shammi & Stuss, 1999; Thompson-Schill, D'Esposito, Aguirre, & Farah, 1997; Wild et al., 2006). Accordingly, we hypothesised that detection of incongruity in our cartoon stimuli would be particularly associated with grey matter volume in this region. Antero-medial and ventral temporal lobe areas and their inferior frontal lobe projections are likely to be engaged in humour comprehension, resolution of incongruity and semantic (including social conceptual) evaluation (Bartolo et al., 2006; Chan, Chou, Chen, Yeh, et al., 2012; Mobbs et al., 2003; Moran et al., 2004; Samson, Hempelmann, Huber, & Zysset, 2009; Samson, Zysset, & Huber, 2008; Zahn, Moll, Iyengar, et al., 2009; Zahn, Moll, Paiva, et al., 2009). We therefore hypothesised a grey matter correlate of humour category processing (familiar versus novel cartoon scenarios) in this region. Ventromedial prefrontal cortex and anterior cingulate have been implicated in linking salient (especially, apparently incompatible or surprising) sensory and cognitive features of humorous stimuli with emotional coding of ‘funniness’ and more specifically in the analysis of mental states embodied in humour (Coulson & Kutas, 2001; Du et al., 2013; Kohn, Kellermann, Gur, Schneider, & Habel, 2011). Therefore, we hypothesised a grey matter correlate in this region for the processing of novel cartoon scenarios that might entail a psychological perspective shift.

[Petter]

https://www.sciencedirect.com/scienc...10945215002695

Laughter is a complex motor behavior that, typically, expresses mirth. Despite its fundamental role in social life, knowledge about the neural basis of laughter is very limited and mostly based on a few electrical stimulation (ES) studies carried out in epileptic patients. In these studies laughter was elicited from temporal areas where it was accompanied by mirth and from frontal areas plus an anterior cingulate case where laughter without mirth was observed. On the basis of these findings, it has been proposed a dichotomy between temporal lobe areas processing the emotional content of laughter and anterior cingulate cortex (ACC) and motor areas responsible of laughter production. The present study is aimed to understand the role of ACC in laughter. We report the effects of stimulation of 10 rostral, pregenual ACC (pACC) patients in which the ES elicited laughter. In half of the patients ES elicited a clear burst of laughter with mirth, while in the other half mirth was not evident. This large dataset allow us to offer a more reliable picture of the functional contribute of this region in laughter, and to precisely localize it in the cingulate cortex. We conclude that the pACC is involved in both the motor and the affective components of emotions, and challenge the validity of a sharp dichotomy between motor and emotional centers for laughing. Finally, we suggest a possible anatomical network for the production of positive emotional expressions.

[Petter]

https://www.sciencedirect.com/scienc...53811923002288

Laughter and crying are universal signals of prosociality and distress, respectively. Here we investigated the functional brain basis of perceiving laughter and crying using naturalistic functional magnetic resonance imaging (fMRI) approach. We measured haemodynamic brain activity evoked by laughter and crying in three experiments with 100 subjects in each. The subjects i) viewed a 20-minute medley of short video clips, and ii) 30 min of a full-length feature film, and iii) listened to 13.5 min of a radio play that all contained bursts of laughter and crying. Intensity of laughing and crying in the videos and radio play was annotated by independent observes, and the resulting time series were used to predict hemodynamic activity to laughter and crying episodes. Multivariate pattern analysis (MVPA) was used to test for regional selectivity in laughter and crying evoked activations. Laughter induced widespread activity in ventral visual cortex and superior and middle temporal and motor cortices. Crying activated thalamus, cingulate cortex along the anterior-posterior axis, insula and orbitofrontal cortex. Both laughter and crying could be decoded accurately (66–77% depending on the experiment) from the BOLD signal, and the voxels contributing most significantly to classification were in superior temporal cortex. These results suggest that perceiving laughter and crying engage distinct neural networks, whose activity suppresses each other to manage appropriate behavioral responses to others’ bonding and distress signals.

Humans have an urgent need to feel belonging to groups and use a multitude of expressions for signifying this. Laughter is a universally recognized positive social expression. It occurs frequently in human social interactions (Sauter et al., 2010; Scott et al., 2015) but is also common among nonhuman primates (Preuschoft, 1992; Ross et al., 2009) and rodents (Panksepp and Burgdorf, 2003). Macaques and chimpanzees use a quiet smile-like gesture to appease aggressive conspecifics, whereas relaxed open-mouth vocalizations are associated with both play behavior and pair formation (Preuschoft, 1992; Waller and Dunbar, 2005). Similarly, humans use quiet smiles for signaling social approval and openness to social interaction (Calvo et al., 2012; Calvo and Nummenmaa, 2015), while laughter is used directly for promoting social bonding (Dunbar, 2012; Scott et al., 2015). Functional and acoustic properties of this kind of play signals in humans resemble those of numerous other animals, most notably other great apes (Winkler and Bryant, 2021).

[Petter]

https://web.archive.org/web/20190226...2c64ba35e3.pdf

The incongruity theory purports that people laugh at things that surprise them or at things that violate an accepted pattern—with a difference close enough to the norm to be nonthreatening, but different enough from the norm to be remarkable. The incongruity theory emphasizes cognition; individuals must have rationally come to understand typical patterns of reality before they can notice differences. A humorous situation must involve the perceiver simultaneously having in mind one view of the situation that seems normal and another view of the situation in which there is a violation of the natural order. This theory has support in neuroimaging research, which shows that the parts of the brain involved in resolving incongruities are activated while processing cartoons.

[...]

The superiority theory proposes that laughing at faulty behavior can reinforce unity among group members. It is believed that superiority humor serves 2 important societal functions: it maintains social order as laughter, rather than aggression, is invoked toward those who refuse to comply with rules and through laughing together at others, it reinforces group unity.

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It is easy to find examples where non-compliance with rules do not elicit laughter.

I think the purpose of laughter is to convey that an unfortunate situation is not causing any real harm so there is no reason to get upset.

[Petter]

https://www.biorxiv.org/content/10.1....518096v1.full

Task-switching is a fundamental cognitive ability which requires animals to update their knowledge of current rules, allowing flexible behaviour in a changing environment. This is often achieved through evaluating discrepancies between observed and expected events. The anterior cingulate cortex (ACC) has a key role in processing such discrepancies, or prediction errors. However, the neural circuit mechanisms underlying task-switching are largely unknown. Here we show that activity in the ACC induced by the absence of expected stimuli is necessary for rapid task-switching. Mice trained to perform a block-wise set-shifting task typically required a single experience of an expectation violation, or prediction error to accurately switch between responding to the same stimuli using distinct rules. Neurons in the ACC explicitly represented these prediction errors, and their activity was predictive of successful one-shot behavioural transitions. Prediction error signals were projection targetspecific, constrained in their spatio-temporal spread across cortex, and heavily disrupted by VIP interneuron perturbation. Optogenetic silencing and single-trial un-silencing revealed that the requirement of the ACC in task-switching was restricted to the epochs when neural prediction error signals were observed. These results reveal a dedicated circuitry promoting the transition between distinct cognitive states.





https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5972193/

The dorsal anterior cingulate cortex (dACC) is proposed to facilitate learning by signaling mismatches between the expected outcome of decisions and the actual outcomes in the form of prediction errors. The dACC is also proposed to discriminate outcome valence—whether a result has positive (either expected or desirable) or negative (either unexpected or undesirable) value. However, direct electrophysiological recordings from human dACC to validate these separate, but integrated, dimensions have not been previously performed. We hypothesized that local field potentials (LFPs) would reveal changes in the dACC related to prediction error and valence and used the unique opportunity offered by deep brain stimulation (DBS) surgery in the dACC of three human subjects to test this hypothesis. We used a cognitive task that involved the presentation of object pairs, a motor response, and audiovisual feedback to guide future object selection choices. The dACC displayed distinctly lateralized theta frequency (3–8 Hz) event-related potential responses—the left hemisphere dACC signaled outcome valence and prediction errors while the right hemisphere dACC was involved in prediction formation. Multivariate analyses provided evidence that the human dACC response to decision outcomes reflects two spatiotemporally distinct early and late systems that are consistent with both our lateralized electrophysiological results and the involvement of the theta frequency oscillatory activity in dACC cognitive processing. Further findings suggested that dACC does not respond to other phases of action-outcome-feedback tasks such as the motor response which supports the notion that dACC primarily signals information that is crucial for behavioral monitoring and not for motor control.





https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3035157/

Convergent evidence for the functional differentiation between the dorsal and ventral ACC/mPFC comes from work on “emotional conflict”. Two recent studies employed a task that required subjects to categorize face stimuli according to their emotional expression (fearful vs. happy), whilst attempting to ignore emotionally congruent or incongruent word labels (HAPPY, FEAR) superimposed over the faces. Emotional conflict, created by a word label that is incongruent with the facial expression, was found to substantially slow reaction times. Moreover, when incongruent trials were preceded by an incongruent trial, reaction times were faster than if incongruent trials were preceded by a congruent trial, an effect that has previously been observed in traditional, non-emotional conflict tasks, such as the Stroop or flanker protocols. According to the “conflict-monitoring model”, this data pattern stems from a conflict-driven regulatory mechanism, where conflict from an incongruent trial triggers an up-regulation of top-down control, reflected in reduced conflict on the subsequent trial. This model allows one to distinguish between brain regions involved in conflict evaluation and those involved in conflict regulation. In the studies of emotional conflict, regions which activated more to post-congruent incongruent trials than post-incongruent incongruent trials, interpreted as being involved in conflict evaluation, included the amygdala, dACC/dmPFC and dorsolateral PFC. The role of dorsal ACC/mPFC areas in detecting emotional conflict is further echoed by other studies of various forms of emotional conflict or interference, the findings of which we plot in Figure 2A.

By contrast, regions more active in post-incongruent incongruent trials are interpreted as being involved in conflict regulation, and prominently include the pgACC. Regulation-related activation in the pgACC was also accompanied by a simultaneous and correlated reduction of conflict-related amygdalar activity and does not seem to involve biasing of early sensory processing streams, but rather the regulation of affective processing itself. These data echo the dorsal-ventral dissociation discussed above with respect to fear expression and extinction in the ACC/mPFC.

[Petter]

https://theconversation.com/the-evol...njoyment-57750

Laughter plays a crucial role in every culture across the world. But it’s not clear why laughter exists. While it is evidently an inherently social phenomenon – people are up to 30 times more likely to laugh in a group than when alone – laughter’s function as a form of communication remains mysterious.

A new study published in the Proceedings of the National Academy of Sciences, and involving a large group of researchers led by Gregory Bryant from UCLA, suggests that laughter may indicate to listeners the friendship status of those laughing. The researchers asked listeners to judge the friendship status of pairs of strangers and friends based on short snippets of their simultaneous laughter. Drawn from 24 different societies, they found that listeners were able to reliably distinguish friends from strangers, based on specific acoustic characteristics of the laughter.

In order to unravel how this is possible and what the true meaning of laughter is, we need to delve back into its early origins.



Laughter’s evolutionary past

Spontaneous laughter, which is unintentionally triggered by conversation or events, emerges in the first few months of life, even in children who are deaf or blind. Laughter not only transcends human cultural boundaries, but species boundaries, too: it is present in a similar form in other great apes. In fact, the evolutionary origins of human laughter can be traced back to between 10 and 16m years ago.

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. As our ancestors began to live in larger and more complex social structures, the quality of relationships became crucial to survival. The process of evolution would have favoured the development of cognitive strategies that helped form and sustain these cooperative alliances.

Laughter probably evolved from laboured breathing during play such as tickling, which encourage cooperative and competitive behaviour in young mammals. This expression of the shared arousal experienced through play may have been effective in strengthening positive bonds, and laughter has indeed been shown to prolong the length of play behaviours in both children and chimpanzees, and to directly elicit both conscious and unconscious positive emotional responses in human listeners.



Laughter as a social tool

The emergence of laughter and other primal vocalisations was at first intimately tied to how we felt: we only laughed when aroused in a positive way, just as we cried only when distressed, or roared only when angry. The key development came with the ability to vocalise voluntarily, without necessarily experiencing some underlying pain, rage, or positive emotion. This increased vocal control, made possible as our brains grew more complex, was ultimately vital in the development of language. But it also allowed us to consciously mimic laughter (and other vocalisations), providing a deceptive tool to artificially quicken and expand social bonds – and so increase survival odds.

The idea that this volitional laughter also has an evolutionary origin is reinforced by the presence of similar behaviour in adult chimpanzees, who produce laugh imitations in response to the spontaneous laughter of others. The fake laughter of both chimpanzees and humans develops during childhood, is acoustically distinct from its spontaneous counterpart, and serves the same social bonding function.

Today, both spontaneous and volitional laughter are prevalent in almost every aspect of human life, whether sharing a joke with a mate or during polite chitchat with a colleague. However, they’re not equivalent in the ear of beholder. Spontaneous laughter is characterised by higher pitch (indicative of genuine arousal), shorter duration and shorter laugh bursts compared to volitional laughter. Researchers recently demonstrated that human listeners can distinguish between these two laugh types. Fascinatingly, they also showed that if you slow down and adjust the pitch of volitional laughter (to make it less recognisable as human) listeners can distinguish it from animal vocalisations, whereas they cannot do the same for spontaneous laughter, whose acoustic structure is far more similar to nonhuman primate equivalents.



Friend or stranger?

It’s this audible difference that is demonstrated in the paper by Bryant and his colleagues. Friends are more likely to produce spontaneous laughs, while strangers who lack an established emotional connection are more likely to produce volitional laughter.

The fact that we can accurately perceive these distinctions means that laughter is to some extent an honest signal. In the neverending evolutionary arms race, adaptive strategies for deception tend to co-evolve with strategies to detect that deception. The acoustic characteristics of authentic laughter are therefore useful cues to the bonds between and status of members of a group. This is something that may have aided decision-making in our evolutionary past.

However, the study found that judgement accuracy was on average only 11% higher than chance. Perhaps this is partially because some strangers may have produced spontaneous laughs and some friends volitional laughs, but it’s clear that imitating authentic emotional laughter is a valuable deceptive tool for social lubrication. One need only witness the contagious effects of canned laughter to see how true this is.
In the complex reality of modern human social interaction, laughs are often aromatic blends of the full-bodied spontaneous and dark but smooth volitional types, further blurring the boundaries. Regardless, the goal is the same and we will most likely find ourselves becoming fonder of those we share the odd chuckle with.

John Cleese once said: “Laughter connects you with people. It’s almost impossible to maintain any kind of distance or any sense of social hierarchy when you’re just howling with laughter.” He might just have hit the nail on the head – even when we’re faking it.

[Petter]

https://link.springer.com/article/10...19-022-00413-6

In 2005, Gervais and Wilson wrote a compelling treatise on the nature of humor and laughter in The Quarterly Review of Biology arguing for the existence of two unique neural laughter pathways. According to Gervais and Wilson (2005), “Duchenne” laughter evolved from the play displays of primates and thus reflects genuine positive affect. This type of laughter is spontaneous, involuntary, and emotional, and originates in older subcortical brain regions such as the brain stem and limbic system. In contrast, “Non-Duchenne” laughter is a more recent evolutionary development that can be employed strategically and is produced in neocortical areas. Given the volitional nature of “Non-Duchenne” laughter, it can serve many functions, from polite social glue which facilitates social bonding, to mocking insult which corrodes social relationships.

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A group of friends have gathered for a dinner party. Jane accidentally stumbles and drops a tray, and her friends burst out laughing. Did she break a social rule? No, of course not, everybody stumbles from time to time.

“Non-Duchenne” laughter is compatible with superiority theory, though.

[Petter]

A.

anger/annoyance <--> it is shameful and it breaks a social rule

laughter <--> it is shameful but it does not break a social rule



B.

laughter <--> teasing (play)

[Petter]

https://royalsocietypublishing.org/d...rsbl.2020.0370

If teasing is more playful and humorous, the teasing event may be mutually enjoyable for both teaser and recipient, and potentially lead to greater closeness (e.g. [10,11]). Accordingly, the proposed functions of teasing are highly diverse and range from gaining social status to enforcing social norms, resolving conflicts and enhancing interpersonal relationships [2–12].

From a psychological perspective, playful teasing, i.e. behaviour that sits on the playful, non-aggressive end of the teasing spectrum, is particularly interesting for two reasons. First, in contrast with other, more obviously aggressive forms of teasing, playful teasing is highly ambiguous. Thus, it most likely involves ‘mind-reading’ skills on both the side of the teaser and the recipient. For playful teasing to be successfully interpreted as affiliative rather than aggressive, the teaser, to some extent, has to understand the recipient's expectations and predict their likely reaction. Likewise, the recipient needs to draw accurate inferences and correctly identify the teaser's intent as affiliative, looking beyond any mildly abrasive behavioural elements. In line with the hypothesis that playful teasing is a cognitively complex form of teasing, studies have shown that teasing is viewed as a potentially positive social interaction only by older children and adolescents. Younger children, by contrast, recognized only the negative sides of teasing [9,12,13]. The second reason playful teasing is interesting psychologically is that it has potential to create mutual amusement. A shared humorous experience is an interaction of positive affective valence and may strengthen social bonds [14–16]. Hence, playful teasing is noteworthy because of its implications for higher socio-cognitive abilities, as well as its potential relevance to the origins and functions of humour.

In contrast with studies showing that only older children interpret teasing behaviour as positive, research on preverbal infants suggests that some forms of non-verbal playful teasing appear before a child's first birthday. Reddy & coworkers [17–21] conducted a series of observational and interview studies and found evidence for positive teasing behaviour in infants as young as 8 months. They described three types of playful teasing in infants: offer and withdrawal of objects or the self (e.g. offering the parent an object and quickly pulling back as the parent reaches for it), provocative non-compliance (e.g. attempting to perform a prohibited action or refusing to perform an expected behaviour) and disrupting others' activities (e.g. taking objects from others when they engage with them; also see, e.g. [22–24] for similar findings in toddlers). Typically, infants repeated these acts several times, all while looking and smiling at the recipient, waiting for an emotional reaction. Infants seemed to seek positive reactions; acts that led to distress in the recipient were rarely repeated [18]. In these exchanges, which typically occurred in moments of neutrality or boredom [21], infants appeared to use teasing to explore limits of newly acquired skills or social agreements, as well as to invite and maintain playful and mirthful interactions [21,23–25].

What these types of infant teasing have in common, and what differentiates them from other types of play initiation, is that the teaser performs an unexpected act, apparently deliberately violating the recipient's expectations, mutual understandings or shared conventions in order to provoke a reaction [21,24–27]. From a socio-cognitive point of view, these behaviours are particularly intriguing, because the ability to manipulate others’ expectations presumably requires relatively sophisticated inferences regarding others' actions and mental states [18,25,26]. For instance, in an offer-withdrawal event, the infant seems not only to anticipate that the recipient will reach for an offered object, but also that she will react with surprise if the offer is withdrawn. The infant seems to be aware of a set of behavioural norms and anticipates what actions would violate those norms and, thus, also violate the recipient's expectations. The infant, therefore, seems to actively create expectations in the other in order to playfully disrupt them. Structurally, this sequence resembles a simple joke, with a familiar setup (the offer) and a surprising punch line (the withdrawal). Like most jokes, playful teasing appears enjoyable for both parties. It relies on an understanding of the familiar event's structure and an appreciation of the incongruous nature of the punch line (e.g. [28,29]). Early forms of joking behaviour in infants described in other studies [26,27,30] also involve playing with rules and expectations (e.g. putting inappropriate objects, such as sponges, in their mouths, while laughing and looking for a reaction [27]).

Importantly, infants can also be knowing recipients of playful teasing and react with laughter when parents do absurd things in an affiliative context, such as drinking from the infant's milk bottle [21,24,31]. Again, what infants seem to find amusing in others' behaviour reveals their awareness of expected (and unexpected) ways to behave. Playful teasing involving the violation of other's expectations might be an important developmental marker of the awareness of other minds and behavioural norms and might represent one of the earliest forms of humour.

The occurrence of playful teasing in preverbal human infants suggests that language is not a prerequisite for this type of behaviour and, thus, opens up intriguing questions about the evolutionary roots of this multifaceted phenomenon. Is playful teasing an early developmental indicator of humans’ unique socio-cognitive skills? Or is it an evolutionarily old behaviour that we might share with other animals, most notably our closest living relatives, the non-human great apes? Answering these questions will help us to develop a better understanding of apes' socio-cognitive capacities and give us intriguing insights into the phylogenetic origins of humour.

[Petter]

C.

incongruity theory + "emotional conflict" (the expected emotion vs. the actual emotion)

[Petter]

https://www.bbc.com/future/article/2...h-when-tickled

What is it about a tickle that makes us giggle? And why can’t we tickle ourselves? Greg Foot explains all.

When you're touched, the nerve endings under your top layer of skin, or epidermis, send electrical signals to the brain. When we are tickled the somatosensory cortex picks up the signals to do with pressure, but the anterior cingulated cortex also analyses the signals. This part of the brain governs pleasurable feelings.

Evolutionary biologists and neuroscientists believe that we laugh when we are tickled because the part of the brain that tells us to laugh when we experience a light touch, the hypothalamus, is also the same part that tells us to expect a painful sensation. Laughing when tickled in our sensitive spots (under the arms, near the throat and under our feet) could be a defensive mechanism. Research suggests that we have evolved to send this signal out to show our submission to an aggressor, to dispel a tense situation and prevent us from getting hurt.

So why can't we tickle ourselves? The cerebellum at the back of the brain tells you that you're about to self-tickle so the brain doesn't waste up precious time interpreting the signals from the tickle.

Bonus fact: Gorillas laugh like us when they're tickled. Rats laugh when they're tickled too, but they giggle at 50kHz, which is out of our audio range.





https://www.theswaddle.com/the-scien...-make-us-laugh

There are some functional, albeit not comprehensively researched, theories as to why these reflex responses accompany the process of being tickled; one, given by researchers at the University of California, San Diego in a study, is “[the] tickle evolved to promote protection of areas that would be most vulnerable during arm-to-arm combat. The idea is that ticklishness in such areas motivates one to protect these areas and thereby confers an adaptive advantage (i.e. increased one’s ability to survive and reproduce). This provides a possible explanation for the pulling away and fending off movements frequently encountered during tickling.”

Researchers add, however, that this theory doesn’t explain why our arms or hands are not ticklish, which logically are the most vulnerable to getting maimed in this hypothetical combat situation. Another theory they offer is that tickling, in modern combat-free society at least, is often carried out between intimate friends and family. When accompanied with smiling or laughter, it creates positive associations within the interaction and can contribute to social bonding between the tickle participants.

Laughter while being tickled, however, needs to be taken with a grain of salt, as it may be a conditioned response, according to the UCSD study. It says that when children are tickled in the context of play, they learn to laugh because of social cues given by those who are tickling them, which happens usually in jest and in a playful manner. “This repeated pairing could lead to Pavlovian conditioning whereby laughter then becomes associated with tickling movements, even when not paired with other humorous situations,” according to the study. “Another possibility is that children laugh when tickled because of the laughter of the tickler which creates some contagious loop (e.g., a parent’s laughter causes the child to laugh which increases the parent’s laughter and so on).” Another 1940s study, however, in which a father wore a mask (so as to not betray any of the above cues) tickled his two babies, the infants still laughed, which led him to conclude that tickling may not be a conditioned response, but an inherently natural one.





https://www.news24.com/life/archive/...ckled-20160323

Dr Grossman, in a Royal Institution’s video on the science behind tickling, explains that we laugh when we’re tickled because "both tickling and laughing activates the Rolandic operculum – a part of the brain that controls facial movement as well as vocal and emotional reactions".

Moreover, Dr van Vuuren says the area of your brain involved in laughing at a funny joke is "not the same as the area associated with laughter when being tickled".

Scientists believe the reason for this difference is because tickling also activates the hypothalamus, which controls body temperature, hunger, tiredness, sexual behaviour and instinctive reactions like the “fight or flight” mechanism.

Even stranger, stimulating the hypothalamus helps the body anticipate pain, say neuroscientists at the University of Tübingen in Germany, which might explain why someone may accidentally lash out at their tickler.

They believe our response to tickling goes back to earliest human evolution, and that it has become a defensive mechanism to indicate submissiveness, calm a tense situation and prevent us from getting hurt.





https://www.nbcnews.com/id/wbna51846086

Both ticklish laughter and voluntary laughter activated the Rolandic operculum brain region, which is located in the primary sensory-motor cortex and is involved in movements of the face; both laughter types were also linked to activity in brain regions involved in vocal emotional reactions, such as crying.

However, only ticklish laughter activated the hypothalamus, a part of the brain involved in regulating many functions, including visceral reactions, the researchers said.

Ticklish laughter also activated parts of the brain thought to be involved in anticipation of pain, which supports the idea that people who are tickled react defensively, the researchers said.

Ticklish laughter appeared to activate the same brain networks seen in earlier studies of humorous laughter. However, humorous laughter also activates an area of the brain involved in "higher order" functions, as well as a part of the brain called the nucleus accumbens, which is thought to be part of the brain's "pleasure center." Ticklish laughter did not activate these areas.

The results, which will be detailed in the June issue of the journal Cerebral Cortex, confirm the idea that ticklish laughter is a "building block" of humorous laughter — an idea first proposed by Charles Darwin and Ewald Hecker in the late 1800s, the researchers noted.





https://academic.oup.com/cercor/arti.../6/1280/426218

The burst of laughter that is evoked by tickling is a primitive form of vocalization. It evolves during an early phase of postnatal life and appears to be independent of higher cortical circuits. Clinicopathological observations have led to suspicions that the hypothalamus is directly involved in the production of laughter. In this functional magnetic resonance imaging investigation, healthy participants were 1) tickled on the sole of the right foot with permission to laugh, 2) tickled but asked to stifle laughter, and 3) requested to laugh voluntarily. Tickling that was accompanied by involuntary laughter activated regions in the lateral hypothalamus, parietal operculum, amygdala, and right cerebellum to a consistently greater degree than did the 2 other conditions. Activation of the periaqueductal gray matter was observed during voluntary and involuntary laughter but not when laughter was inhibited. The present findings indicate that hypothalamic activity plays a crucial role in evoking ticklish laughter in healthy individuals. The hypothalamus promotes innate behavioral reactions to stimuli and sends projections to the periaqueductal gray matter, which is itself an important integrative center for the control of vocalization. A comparison of our findings with published data relating to humorous laughter revealed the involvement of a common set of subcortical centers.





https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6847157/

In analogy to the appreciation of humor, that of tickling is based upon the re-interpretation of an anticipated emotional situation. Hence, the anticipation of tickling contributes to the final outburst of ticklish laughter. To localize the neuronal substrates of this process, functional magnetic resonance imaging (fMRI) was conducted on 31 healthy volunteers. The state of anticipation was simulated by generating an uncertainty respecting the onset of manual foot tickling. Anticipation was characterized by an augmented fMRI signal in the anterior insula, the hypothalamus, the nucleus accumbens and the ventral tegmental area, as well as by an attenuated one in the internal globus pallidus. Furthermore, anticipatory activity in the anterior insula correlated positively with the degree of laughter that was produced during tickling. These findings are consistent with an encoding of the expected emotional consequences of tickling and suggest that early regulatory mechanisms influence, automatically, the laughter circuitry at the level of affective and sensory processing. Tickling activated not only those regions of the brain that were involved during anticipation, but also the posterior insula, the anterior cingulate cortex and the periaqueductal gray matter. Sequential or combined anticipatory and tickling-related neuronal activities may adjust emotional and sensorimotor pathways in preparation for the impending laughter response.

[...]

In the rat, the lateral hypothalamus is involved in vocalizations that are related to the expression of positive emotions (Burgdorf et al., 2007), notably to those that occur in the context of tickling and play (Roccaro-Waldmeyer et al., 2016). In humans, the lateral hypothalamus is activated during the processing of humor (Watson et al., 2007; Schwartz et al., 2008) and of ticklish laughter (Wattendorf et al., 2013). Both the hypothalamus and the PAG receive projections from the insula (Reep and Winans, 1982); the latter represents a primary cortical relay for tactile afferents that mediate affective information (Olausson et al., 2002). The functions of the anterior insula (AI) are believed to be implicated in the triggering of human laughter (Watson et al., 2007; Holstege and Subramanian, 2016). Interestingly in this context, the AI not only senses the physiological condition of the body and related feelings, but also estimates the impact of an upcoming stimulation on this bodily state (Craig, 2002, 2009). Furthermore, the AI is believed to form a part of a limbic-related processing network that produces an affective state in response to the emotional significance of a stimulus, which is then automatically relayed to regulate emotional behavior [(Phillips et al., 2003), see also Figure 1]. Along these lines, activity in this cortical region occurs during the experience of tickling or a pleasant touch and during the anticipation of these sensations (Lovero et al., 2009; Lucas et al., 2015). However, a possible involvement of downstream regions, such as the hypothalamus and the PAG, has not been considered thus far. Our own investigations have permitted us to demonstrate activity that is associated with ticklish laughter in the AI/hypothalamic/PAG axis (Wattendorf et al., 2013; Wattendorf et al., 2016). However, in these former studies, no attempt was made to locate the sites of activity that are associated with the preceding anticipatory processes. It was with this aim in view that the present study was conducted. The partial brain volume targeted included the three aforenamed key nodes of the emotional motor system. By focusing on the AI, the hypothalamus and the PAG, we have now distinguished the processes of anticipation from those that are relevant during tickling.

[...]

The posterior insular cortex contains primary interoceptive afferences that the anterior portions integrate with cognitive and limbic-related information (Craig, 2002; Critchley, 2005; Craig, 2009). This process represents the basis of emotional experiences and has been associated with a broad spectrum of functional conditions (Kurth et al., 2010). The anterior insular cortex (AI) is believed to comprise a portion of the neuronal network that produces an affective state corresponding to an emotional stimulation (Phillips et al., 2003). Interestingly in this context, an anticipation of the averse consequences of a stimulus invariably leads to an activation of the AI and, at the same time, is associated with autonomous excitement and behavioral changes (Etkin and Wager, 2007). Indeed, the prediction of an affective state in the absence of a peripheral input appears to be a key role of the AI (Paulus and Stein, 2006). This observation may also apply to tickling or a pleasant touch: although activity in the AI has been observed during the sensory stimulation itself (Carlsson et al., 2000; Morrison, 2016), this region appears to be specifically implicated in paradigms that signal an upcoming experience of the related bodily sensations (Lovero et al., 2009). Our data support the implication that the AI is involved in the anticipation of tickling (A). The functions that involve its right ventral portion permit the drawing of further conclusions.

One of the characteristics of tickling is that during the act itself, it is re-interpreted as a harmless stimulus. The continuous up-dating of information appertaining to the actual situation is assumed to be supported by the von Economo neurons (VEN) in the ventral portion of the AI (von Economo, 1926), which have been implicated in the rapid, highly integrated representations of an emotional experience (Craig, 2009). In a previous study, the mechanism that underlies the recognition and the re-appraisal of humorous stimuli has indeed been explained by this process (Watson et al., 2007). The ventral AI [agranular, see (Evrard et al., 2014)] is functionally involved in an affective state that is generated according to an emotional rather than a cognitive input (Kurth et al., 2010). This region appears to be the seat of feelings that are not defined or interpreted (Wager and Barrett, 2004), such as those that are associated with the experience of one of the basic emotions (Damasio et al., 2000) or a state of intensified drive [e.g. the craving for food (Pelchat et al., 2004)]. The ventral AI also participates in the regulation of peripheral physiological changes that are related to affective states (Mutschler et al., 2009). Notably, neuronal activity that is restricted to the right ventral AI signalizes higher sympathetic arousal (Critchley et al., 2000), as gauged, for example, by the concomitant change in skin conductance that occurs during the experience of positive emotions (Kuniecki et al., 2003). Moreover, in the rat, efferent sympathetic projections from the agranular and the dysgranular insular cortices have been traced (Cechetto and Chen, 1990; Yasui et al., 1991). This discovery serves as more than circumstantial evidence of the insula’s involvement in regulation via the sympathetic nervous system, which has been verified in humans: unexpected cardiac events following insular stroke are deemed to be associated with the sympathetic role of the right AI (Tokgozoglu et al., 1999). Hence, during the anticipation of tickling, the dextroventral AI possibly acts as a dynamic point of reference (Gu et al., 2013) in the automatic regulation of the laughter circuitry.

[Petter]

(see post #453, #455, #456 and #472)



https://www.cell.com/neuron/fulltext...273(22)00549-9

The orbitofrontal cortex (OFC) and the caudate nucleus (CdN) have both been linked to decision making, although the path they took toward entering decision-making models is quite different. The importance of OFC, or more generally, the frontal lobe, became clear long before modern brain-mapping techniques were developed. This insight came from Phineas Gage’s surprising recovery from a severe head injury in 1848 which eliminated parts of his OFC and—among other things—left him with poor decision-making skills (Bigelow, 1850). The CdN, on the other hand, was originally considered part of motor processes but has received more and more attention in the past decades for its involvement in memory, learning, and eventually decision making.

[...]

In contrast to CdN, the activity of about half of the recorded neurons in OFC could be predicted only by max value and not by choice direction (except for a handful of neurons). The authors replicate the previously reported “flip-flopping,” which refers to the back and forth between representing the value of chosen and unchosen options while the monkeys are looking at the pictures. Interestingly, these representations were independent of the monkeys’ eye movements. As in CdN, response times were predicted by decoding strength where decoding was synced with picture onset rather than response onset. In summary, OFC encodes the value of both options but not orienting behavior toward them. This is consistent with a deliberation process, where individual neurons sequentially represent the value of both the chosen and unchosen options.





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

A related, though slightly different idea is that hyperactivation of the OFC, ACC, and caudate nucleus simply reflects the need to inhibit compulsive behavior during the scan (Peterson, 2003). This idea is supported by the finding that the ACC and the head of the caudate nucleus are activated when patients with Tourette’s syndrome (TS) voluntarily inhibit their tics (Peterson et al., 1998).





https://www.researchgate.net/figure/..._fig5_14132592

https://i.imgur.com/eH8NiBC.jpg

The medial OFC-basal ganglia loop.

ACA = anterior cingulate area
AMG = amygdala
CD = caudate nudeus
ENT = entorhinal cortex
ITG = inferior temporal gyros
OFC = orbital frontal cortex
STG = superior temporal gyrus
Thal = thalamus
VS = ventral striatum

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

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

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

[...]

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

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

[Petter]

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

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

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

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

The fMRI experiment demonstrated that frustration can affect activation in structures which showed increased BOLD signal in acute stress studies: striatum, cingulate cortex, insula, middle frontal gyrus, and precuneus and in structures engaged in tactile discrimination task: SI and SII.

Caudate, putamen, and insula composed the biggest cluster of activation during the Braille discrimination task after frustration induction (compared to the same task before the frustration induction). It is known that dorsal striatum (caudate) activation contributes importantly to stress and negative affect processing (Dias-Ferreira et al., 2009; Seo et al., 2014). Furthermore, Schwabe and Wolf (2012) showed that stress alters the engagement of multiple memory systems in the human brain. They stated that stress impairs the hippocampus-dependent memory system and allows the striatum to control behavior. It results in a shift toward “procedural” learning after the stress appears. This kind of shift is proved to be adaptive, because it rescues the task performance after the stress (Schwabe and Wolf, 2012). This effect gives an insight into the lack of decrease in performance after the appearance of frustration observed in this study.

------

Frustration does not involve the amygdala so it is not a basic emotion.

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3 basic emotions: excitement, anger and fear

[Petter]

human needs


1. physiological needs: air, water, food, warmth, sleep, sex, avoid pain, avoid disgust <--> pleasure and misery


2. avoid threats <--> fear


3. defend resources <--> aggression/anger


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


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


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


7. play <--> laughing


8. meaningfulness <--> happiness and sadness

[Petter]

basic emotions: survival needs + approach/avoidance + amygdala and hypothalamus

[Petter]

https://onlinelibrary.wiley.com/doi/....1002/ab.22092

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

frustration and humiliation (esteem needs) ---> aggression

[Petter]

excitement:


1)

appetitive impulsivity <--> hunting

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.

2)

control/orientation (achieve goals and get rewarded)

3) both

[Petter]

avoid threats <--> attachment (love and mutual care)


defend resources <--> dominance (social hierarchy)


appetitive impulsivity and/or control/orientation (achieve goals and get rewarded) <--> social play

[Petter]

(see post #465)


https://pubmed.ncbi.nlm.nih.gov/28918358/

The involvement of the amygdala in aggression is supported by overwhelming evidence. Frequently, however, the amygdala is studied as a whole, despite its complex internal organization. To reveal the role of various subdivisions, here we review the involvement of the central and medial amygdala in male rivalry aggression, maternal aggression, predatory aggression, and models of abnormal aggression where violent behavior is associated with increased or decreased arousal. We conclude that: (1) rivalry aggression is controlled by the medial amygdala; (2) predatory aggression is controlled by the central amygdala; (3) hypoarousal-associated violent aggression recruits both nuclei, (4) a specific upregulation of the medial amygdala was observed in hyperarousal-driven aggression. These patterns of amygdala activation were used to build four alternative models of the aggression circuitry, each being specific to particular forms of aggression. The separate study of the roles of amygdala subdivisions may not only improve our understanding of aggressive behavior, but also the differential control of aggression and violent behaviors of various types, including those associated with various psychopathologies.


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https://i.imgur.com/Npbu2Hf.jpg


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https://onlinelibrary.wiley.com/doi/...1111/jnc.15301

https://www.sciencedirect.com/scienc...89004222017692

https://www.cambridge.org/core/journ...8E4281D712592A

https://www.frontiersin.org/journals...4.1364268/full

[Petter]

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

The amygdala consists of a range of interconnected nuclei having a common output through the central nucleus and the bed nucleus of the stria terminalis (Bnst). In particular, the medial amygdala (Mea) and the Bnst have been implicated in offensive aggression. The medial amygdala receives direct input from the accessory olfactory bulb, which, in turn, is the main relay station of olfactory information originating from the vomeronasal organ (Figure 1). This part of the olfactory system is specialized in the detecting species-specific chemosensory signals. Hence, olfactory stimuli that are relevant for social behavior in general have a dedicated entrance into the brain, reaching the medial amygdala almost directly. The medial amygdala is characterized by a high density of both estrogen and androgen receptors. These receptors are located, in particular, on neurons that produce the neuropeptide vasopressin (AVP). The synthesis of AVP in these neurons is enhanced by testosterone. This testosterone-dependent vasopressinergic system is sexually dimorphic and projects to the lateral septal area. The medial amygdala has an important function in the modulation of social behavior based on social experience.

[...]

The amygdala, which consists of a complex of nuclei located in the rostral aspect of the temporal lobe, has received more attention than any other limbic structure with respect to its relationship to emotional behavior. These studies have revealed that the amygdala is not uniform in its effects on aggression and rage. Instead, the effects are dependent on both the form of aggression and region of amygdala considered.

Excitation of the region of amygdala, including the medial nucleus and medial aspect of the basal complex, in the cat potentiates defensive rage behavior elicited from the medial hypothalamus, whereas excitation of the lateral and central nuclei or lateral aspect of the basal complex suppresses this response. The potentiating effects of the medial amygdala are mediated over the stria terminalis, which projects to the bed nucleus of the stria terminalis and rostral half of the medial hypothalamus, including the dorsomedial region and shell of the ventromedial nucleus. A primary neurotransmitter of this pathway has been identified as substance P (SP), acting on neurokinin (NK)-1 receptors in the medial hypothalamus. In contrast, excitation of the medial amygdala suppresses predatory attack behavior elicited from the lateral hypothalamus. Suppression is manifest via a disynaptic pathway in which the first limb includes the stria terminalis projection to the medial hypothalamus and the second a GABAergic (inhibitory) neuron projecting from the medial to lateral hypothalamus. The inhibitory effects of the amygdala on defensive rage behavior are mediated through a descending projection to the midbrain PAG. The neurotransmitter has been shown to be enkephalin acting through μ-opioid receptors in the PAG. In a parallel manner, excitation of the lateral amygdala potentiates predatory attack. Although the pathway has not been experimentally identified, it is likely to include fibers of the ventral amygdalofugal pathway projecting to the lateral hypothalamus.

[Petter]

central amygdala: approach or avoidance (caudate nucleus and putamen) ... see post #509 and #510

medial amygdala: direct interaction with a predator, a rival, a partner or cubs ... see post #511 and #512

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https://i.imgur.com/vvCCr2g.png

https://i.imgur.com/XjXJau5.jpg

[Petter]

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

These findings might have pointed out the role of the medial amygdala in response to the social interaction; however, further analysis of the results of studies investigating the pattern of genes expression after various behavioral tests shows that the medial amygdala is also active during very different, not clearly social tasks, e.g., fear conditioning, two-way avoidance training, exposure to the elevated mazes, or nose-poking for water reward. In aggregate, one can come to the conclusion that the expression of gene activity markers in the medial amygdala is evoked by every novel aspect of the experimental situation (see Ref. 88).

[Petter]

https://www.sciencedirect.com/scienc...31938473901261

Predatory-like biting attack and associated prey-kicking, grooming, and components of threat behavior were elicited by electrical stimulation of different, but partly overlapping areas of the pontine tegmentum in cats. Electrodes producing biting attack and prey-kicking were located in the central tegmentum. The effective area for grooming was located in the dorsolateral tegmentum and extended, with the superior cerebellar peduncle, into the deep fibers of the cerebellum. Electrodes producing threat responses were more widely distributed, but tended to be located ventrally or laterally. The results support the view that the lower brainstem may play an important role in the production of complex species-typical behaviors.

[Petter]

anger ---> aggression

trust, tenderness, love (?) ---> social grooming

[Petter]

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

central amygdala <--> excitement ('wanting') and fear

[Petter]

basolateral amygdala (BLA) + caudate nucleus and putamen <--> approach or avoidance

[Petter]

https://www.sciencedirect.com/scienc...66432823001365

Social stressors negatively impact social function, and this is mediated by the amygdala across species. Social defeat stress is an ethologically relevant social stressor in adult male rats that increases social avoidance, anhedonia, and anxiety-like behaviors. While amygdala manipulations can mitigate the negative effects of social stressors, the impact of social defeat on the basomedial subregion of the amygdala is relatively unclear. Understanding the role of the basomedial amygdala may be especially important, as prior work has demonstrated that it drives physiological responses to stress, including heart-rate related responses to social novelty. In the present study, we quantified the impact of social defeat on social behavior and basomedial amygdala neuronal responses using anesthetized in vivo extracellular electrophysiology in adult male Sprague Dawley rats. Socially defeated rats displayed increased social avoidance behavior towards novel Sprague Dawley conspecifics and reduced time initiating social interactions relative to controls. This effect was most pronounced in rats that displayed defensive, boxing behavior during social defeat sessions. We next found that socially defeated rats showed lower overall basomedial amygdala firing and altered the distribution of neuronal responses relative to the control condition. We separated neurons into low and high Hz firing groups, and neuronal firing was reduced in both low and high Hz groups but in a slightly different manner. This work demonstrates that basomedial amygdala activity is sensitive to social stress, displaying a distinct pattern of social stress-driven activity relative to other amygdala subregions.





https://www.researchgate.net/figure/...fig1_340331033

https://i.imgur.com/4lIl6cI.png

Connections of the medial amygdala (MA) subnuclei with the bed nucleus of the stria terminalis (BNST), other amygdaloid regions, and preoptic-hypothalamic structures. Arrow thickness and direction indicate the relative strength and direction of connections of MAa, MApv, and rostral and caudal levels of MApd with subnuclei of BNST, medial preoptic (MPOA), ventromedial hypothalamic nucleus (VMN) as well as basomedial and central amygdala and other hypothalamic areas (AVPe nucleus-anteroventral periventricular hypothalamic nucleus; premammillary nucleus). Dashed lines indicate the primarily efferent output of MA subnuclei. Intensity of gray shading indicates the relative abundance of steroid hormone receptors. Additional abbreviations as in Fig. 1.





https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4780260/

Anxiety-related conditions are among the most difficult neuropsychiatric diseases to treat pharmacologically, but respond to cognitive therapies. There has therefore been interest in identifying relevant top-down pathways from cognitive control regions in medial prefrontal cortex (mPFC). Identification of such pathways could contribute to our understanding of the cognitive regulation of affect, and provide pathways for intervention. Previous studies have suggested that dorsal and ventral mPFC subregions exert opposing effects on fear, as do subregions of other structures. However, precise causal targets for top-down connections among these diverse possibilities have not been established. Here we show that the basomedial amygdala (BMA) represents the major target of ventral mPFC in amygdala in mice. Moreover, BMA neurons differentiate safe and aversive environments, and BMA activation decreases fear-related freezing and high-anxiety states. Lastly, we show that the ventral mPFC–BMA projection implements top-down control of anxiety state and learned freezing, both at baseline and in stress-induced anxiety, defining a broadly relevant new top-down behavioural regulation pathway.

Human and animal studies have implicated diverse cortical and subcortical regions in anxiety and fear regulation. Interestingly, altered structure and activity correlations between mPFC and amygdala have been reported in patients with anxiety disorders, although the precise causal connections remain unclear. Complexity is suspected, since ventral and dorsal mPFC (vmPFC and dmPFC, respectively) may have opposing roles in fear (vmPFC inhibits dmPFC, and stimulation of vmPFC or dmPFC respectively decreases or increases freezing). Relevant subcortical regions are also complex; inhibitory intercalated cells (ITCs) in amygdala have been hypothesized to be vmPFC targets, and to inhibit fear-promoting cells of the central nucleus of the amygdala, which could be relevant to the decreased freezing caused by electrical stimulation of vmPFC3. In contrast, dmPFC innervates the basolateral amygdala (BLA), and the bulk of the BLA population promotes fear. This model could explain vmPFC–dmPFC functional differences and why lesioning ITCs promotes freezing, but has never directly and precisely been tested.

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vlPFC: ambiguity 1 (objects/patterns)

vmPFC: ambiguity 2 (reward and punishment) ... decision-making

[Petter]

https://www.frontiersin.org/journals...21.752320/full

The human MeA is situated anterior-medial to the central nucleus in the anterior-dorsal part of the amygdala (Sorvari et al., 1996; Schumann and Amaral, 2005), not to be confused with the basomedial amygdala, or the medial aspect of the amygdala (Figure 1). Most of our knowledge of the MeA comes from rodent work, which has shown that it is involved in a wide range of social behaviors (Lehman et al., 1980; Haller, 2018), and is a major constituent of the accessory olfactory system, receiving the bulk of monosynaptic projections from the accessory olfactory bulb (Mohedano-Moriano et al., 2007; Pro-Sistiaga et al., 2007). Within the accessory olfactory system, the MeA plays an important role in processing pheromonal signals and differentiating olfactory social cues including those that carry meaning about sex, age, and danger status (Bergan et al., 2014; Li et al., 2017; Yao et al., 2017; Lee et al., 2021). Social behaviors in rodents are strongly impacted by the main olfactory system (Keshavarzi et al., 2015; Pardo-Bellver et al., 2017), so it is likely that the MeA is involved in the processing of social cues that are encountered through the main olfactory system as well.

In rodents, the MeA is a multisensory area that receives cortically-processed sensory input from visual and auditory modalities (Mosher et al., 2010). The MeA is also involved in generating socially-guided behavioral outputs, including expression of aggression (Kemble et al., 1984; Blanchard and Takahashi, 1988; Newman, 1999; Veening et al., 2005; Lin et al., 2011; Hong et al., 2014; Padilla et al., 2016; Miller et al., 2019; Nordman and Li, 2020), mating behaviors (Rajendren and Moss, 1993; Kondo and Arai, 1995; Lin et al., 2011; DiBenedictis et al., 2012; Ishii et al., 2017), parenting behaviors (Fleming et al., 1980; Numan et al., 1993; Sheehan et al., 2001; Tachikawa et al., 2013; Isogai et al., 2018; Chen et al., 2019; Trouillet et al., 2019), social recognition memory (Ferguson et al., 2001; Gur et al., 2014; Shemesh et al., 2016), self-grooming (Hong et al., 2014), and interspecies defensive behaviors (Choi et al., 2005; Ishii et al., 2017; Li et al., 2017; Miller et al., 2019).

The MeA also plays a critical role in rodent approach-avoidance conflict behavior, both olfactory and non-olfactory mediated. For example, excitotoxic lesioning of the MeA reduces defensive behavior in rats during exposure to a live cat and increases exploratory locomotion (Martinez et al., 2011). Exposure to innate threat stimuli, such as predator odorants and intruder conspecifics, induces Fos expression in the MeA (Kollack-Walker et al., 1999), and distinct subpopulations of MeA neurons have opposing effects on investigation or avoidance of threatening stimuli (Miller et al., 2019). Interestingly, defensive responses are state-dependent, adapting to the fed state of an animal, and evidence suggests that these adaptations specifically involve neurons in the MeA (Padilla et al., 2016). In approach–avoidance conflict, the exploratory drive is essential to maximize an animal’s ability to thrive, whereas avoidance is essential for survival (Elliot, 2006). Findings from the aforementioned studies combine to suggest a critical role for the MeA in mediating this conflict.

Considering that the MeA is a central part of the rodent accessory olfactory system—which humans lack—the role of the MeA in humans is particularly intriguing. Non-human primate work suggests that the MeA’s involvement in social processing is conserved, showing that MeA neurons are responsive to socially important information such as facial expressions, facial identities, pair bonding, and jealousy (Leonard et al., 1985; Brothers et al., 1990; Gothard et al., 2007; Hoffman et al., 2007). Few human studies have specifically delineated the MeA and analyzed signals from it, though it may be involved in perception and processing of emotional faces (Gamer et al., 2010). Large lesions of the human amygdala that include the MeA result in emotional processing deficits, whereas lesions that spare MeA do not (Adolphs et al., 2002; Becker et al., 2012). A combined functional Magnetic Resonance Imaging (fMRI) and Positron Emission Tomography (PET) study found that connectivity between a medial portion of the human amygdala and prefrontal limbic brain regions correlated with dopamine increases in that same network when mothers interacted with their infants (Atzil et al., 2017). However, the medial portion of the amygdala used in that study was based on functional parcellations and likely corresponded to the basomedial amygdala rather than the MeA (Bickart et al., 2012). Other research on the human MeA has implicated it as part of the default mode network (Bickart et al., 2014) and it may be prone to aging and dementia-related cell loss (Herzog and Kemper, 1980; Aghamohammadi-Sereshki et al., 2019). The role of the MeA in human olfaction is virtually unexplored.

Despite this lack of research, the fact that the human olfactory bulb projects monosynaptically to the MeA (Allison, 1954) implicates this subregion in a significant olfactory role which remains to be disambiguated. Odors trigger innate responses in humans (Yeshurun and Sobel, 2010), and humans engage in olfactory-guided social behaviors (Classen, 1992; Ober et al., 1997; Wysocki and Preti, 2004; Wyart et al., 2007; Samuelsen and Meredith, 2009; de Groot et al., 2012; Frumin et al., 2015), despite the lack of an accessory olfactory system (Mast and Samuelsen, 2009; Savic et al., 2009). The neural bases of these behaviors have yet to be identified. The MeA is well-situated to process these behaviors in humans.

[Petter]

https://www.frontiersin.org/journals...21.752320/full

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

Figure 4. Whole-brain resting connectivity of the MeA. Regions of interest include the insula, motor cortex, anterior cingulate cortex, and raphe nuclei.




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

adACC <--> conflict-monitoring

[Petter]

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

One way in which resources in an environment might be unevenly distributed is across time. For example, one foraging location, such as a particular fruit tree, may have held a high value over the last couple of days since fruits have ripened, but a low average value over the last few months, when there were no fruits at all. On the other hand, another location populated by edible insects may have lower value right now, but higher long-term value, because the presence of insects is more regular across seasons. Both neuroimaging studies in humans and single-neuron recording studies in macaques demonstrate that the dACC simultaneously holds multiple representations of value with different time constants (Bernacchia et al., 2011; Cavanagh et al., 2016; Meder et al., 2017; Murray et al., 2014; Seo and Lee, 2009; Spitmaan et al., 2020; Wittmann et al., 2016a). For example, Meder et al. (2017) used fMRI to examine neural activity while people decided whether to repeat a choice or switch to an alternative. They reported that variation in dACC activity was related to variation in choice value. Importantly, however, dACC voxels carried estimates of choice value that were constructed over different timescales (Figure 3A, left). For example, activity in one ACC voxel might reflect whether a choice had been successful and delivered reward on average over the course of many previous trials. However, another voxel’s activity might reflect whether the choice had been successful on just the most recent trials. This means that the ACC constructs multiple estimates of choice value over different timescales.

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https://i.imgur.com/xCRHgU7.jpg

SN (incl. vmPFC and amygdala) ---> CON 1 (task control) ---> CON 2 (premotor processes: pain avoidance/vigilance) ---> action

[Petter]

https://academic.oup.com/cercor/arti...11/2669/284188

Ventromedial prefrontal cortex (VMF) is thought to be important in human decision making, but studies to date have focused on decision making under conditions of uncertainty, including risky or ambiguous decisions. Other lines of evidence suggest that this area of the brain represents quite basic information about the relative “economic” value of options, predicting a role for this region in value-based decision making even in the absence of uncertainty.

[...]

These results argue that VMF plays a necessary role in certain as well as uncertain decision making in humans.

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value of options <--> OFC (?)