Amygdala

It is well established that glucocorticoid hormones, secreted by the adrenal cortex after a stressful event, influence cognitive performance. Some studies have found glucocorticoid-induced memory enhancement. However, many studies have reported impairing effects of glucocorticoids on memory function. This paper reviews recent findings from this laboratory on the acute effects of glucocorticoids in rats on specific memory phases, i.e., memory consolidation and memory retrieval. The evidence suggests that the consequences of glucocorticoid activation on cognition depend largely on the different memory phases investigated. Posttraining activation of glucocorticoid-sensitive pathways involving glucocorticoid receptors enhances memory consolidation in a pattern highly similar to that previously described for adrenal catecholamines. Also, similar to catecholamine effects on memory consolidation, glucocorticoid influences on memory consolidation depend on noradrenergic activation of the basolateral complex of the amygdala and interactions with other brain regions. By contrast, memory retrieval processes are usually impaired with high circulating levels of glucocorticoids or following infusions of glucocorticoid receptor agonists into the hippocampus. The hypothesis is proposed that these apparently dual effects of glucocorticoids on memory consolidation and memory retrieval might be related and that the basolateral complex of the amygdala is a key structure in a memory-modulatory system that regulates, in concert with other brain regions, stress and glucocorticoid effects on both memory consolidation and memory retrieval. ᭧ 2002 Elsevier Science (USA)

Abstract: Neuroimaging research has helped to advance neurobiological models of anxiety disorders. The amygdala is known to play an important role in normal fear conditioning and is implicated in the pathophysiology of anxiety disorders. The amygdala may also be a target for the beneficial effects of cognitive-behavioral and medication treatments for anxiety disorders. In the current paper, we review neuroimaging research pertaining to the role of the amygdala in anxiety disorders and their treatment. Moreover, we discuss the development of new neuroimaging paradigms for measuring aspects of amygdala function, as well as the function of related brain regions. We conclude that such tools hold great promise for facilitating progress in relevant basic neuroscience as well as clinical research domains.

It is well known that stressful experiences may affect learning and memory processes. Less clear is the exact nature of these stress effects on memory: both enhancing and impairing effects have been reported. These opposite effects may be explained if the different time courses of stress hormone, in particular catecholamine and glucocorticoid, actions are taken into account. Integrating two popular models, we argue here that rapid catecholamine and non-genomic glucocorticoid actions interact in the basolateral amygdala to shift the organism into a 'memory formation mode' that facilitates the consolidation of stressful experiences into long-term memory. The undisturbed consolidation of these experiences is then promoted by genomic glucocorticoid actions that induce a 'memory storage mode', which suppresses competing cognitive processes and thus reduces interference by unrelated material. Highlighting some current trends in the field, we further argue that stress affects learning and memory processes beyond the basolateral amygdala and hippocampus and that stress may pre-program subsequent memory performance when it is experienced during critical periods of brain development. (L. Schwabe). the stressful situation and bringing our organism back into balance (i.e., homeostasis). In particular, two systems are mobilized under stress: (i) the fast acting sympathetic nervous system and (ii) the slow hypothalamus-pituitary-adrenal (HPA) axis. Sympathetic nervous system responses include the release of the catecholamines adrenaline and noradrenaline from the adrenal medulla, which cause, for example, increases in heart rate or enhanced blood flow to skeletal muscles and thus prepare the organism for a 'fight-orflight' response. Activation of the HPA-axis leads, via intermediate steps, to the release of glucocorticoids (mainly cortisol in humans, corticosterone in rodents) from the adrenal cortex. Glucocorticoids 0149-7634/$ -see front matter

Brothers (Brothers L. Concepts in Neuroscience 1990;1:27-51) proposed a network of neural regions that comprise the "social brain", which includes the amygdala. Since the childhood psychiatric condition of autism involves deficits in "social intelligence", it is plausible that autism may be caused by an amygdala abnormality. In this paper we review the evidence for a social function of the amygdala. This includes reference to the Kluver-Bucy syndrome (which Hetzler and Griffin suggested may serve as an animal model of autism). We then review evidence for an amygdala deficit in people with autism, who are well known to have deficits in social behaviour. This includes a detailed summary of our recent functional magnetic resonance imaging (fMRI) study involving judging from the expressions of another person's eyes what that other person might be thinking or feeling. In this study, patients with autism or AS did not activate the amygdala when making mentalistic inferences from the eyes, whilst people without autism did show amygdala activity. The amygdala is therefore proposed to be one of several neural regions that are abnormal in autism. We conclude that the amygdala theory of autism contains promise and suggest some new lines of research. ᭧

Music is frequently employed, in the laboratory as well as the cinema, to portray and arouse fear. The neurological structure most commonly associated with fear is the amygdala, and the amygdala is frequently implicated in studies of musical emotion. But not all fears are amygdala-based, nor are all amygdala-based emotions of the “fear” type. Through analyses of laboratory stimuli, Erdmann and Becce’s corpus of early film music, passages from Verdi’s Requiem, and a sequence from the film Jaws, this essay explores both what scary music is in the structural sense and what it does when it encounters the amygdala. The argument is that fear is a messy concept in its mapping onto both music and neural structures like the amygdala. A different manner of affective analysis is envisioned, in which musical structure and affect-associated brain regions are mapped directly onto one another, eliminating the messy middleman of folk-psychological concepts like “scariness” and “fear.” On this (admittedly speculative) model, affect can still be investigated as a contributor to musical experience, but in a potentially more precise, less impressionistic way.

Early global deprivation of institutionalized children may result in persistent specific cognitive and behavioral deficits. In order to examine brain dysfunction underlying these deficits, we have applied positron emission tomography using 2-deoxy-2-[ 18 F]fluoro-D-glucose in 10 children (6 males, 4 females, mean age 8.8 years) adopted from Romanian orphanages. Using statistical parametric mapping (SPM), the pattern of brain glucose metabolism in the orphans was compared to the patterns obtained from two control groups: (i) a group of 17 normal adults (9 males, 8 females, mean age 27.6 years) and (ii) a group of 7 children (5 males and 2 females, mean age 10.7 years) with medically refractory focal epilepsy, but normal glucose metabolism pattern in the contralateral hemisphere. Consistent with previous studies of children adopted from Romanian orphanages, neuropsychological assessment of Romanian orphans in the present study showed mild neurocognitive impairment, impulsivity, and attention and social deficits. Comparing the normalized glucose metabolic rates to those of normal adults, the Romanian orphans showed significantly decreased metabolism bilaterally in the orbital frontal gyrus, the infralimbic prefrontal cortex, the medial temporal structures (amygdala and head of hippocampus), the lateral temporal cortex, and the brain stem. These findings were confirmed using a region-of-interest approach. SPM analysis showed significantly decreased glucose metabolism in the same brain regions comparing the orphans to the nonepileptic hemisphere of the childhood epilepsy controls. Dysfunction of these brain regions may result from the stress of early global deprivation and may be involved in the long-term cognitive and behavioral deficits displayed by some Romanian orphans.

Brothers (Brothers L. Concepts in Neuroscience 1990;1:27-51) proposed a network of neural regions that comprise the "social brain", which includes the amygdala. Since the childhood psychiatric condition of autism involves deficits in "social intelligence", it is plausible that autism may be caused by an amygdala abnormality. In this paper we review the evidence for a social function of the amygdala. This includes reference to the Kluver-Bucy syndrome (which Hetzler and Griffin suggested may serve as an animal model of autism). We then review evidence for an amygdala deficit in people with autism, who are well known to have deficits in social behaviour. This includes a detailed summary of our recent functional magnetic resonance imaging (fMRI) study involving judging from the expressions of another person's eyes what that other person might be thinking or feeling. In this study, patients with autism or AS did not activate the amygdala when making mentalistic inferences from the eyes, whilst people without autism did show amygdala activity. The amygdala is therefore proposed to be one of several neural regions that are abnormal in autism. We conclude that the amygdala theory of autism contains promise and suggest some new lines of research. ᭧

Background: Although recent neuroimaging and therapeutic transcranial magnetic cortex stimulation (TMS) studies suggest imbalance between left and right dorsolateral prefrontal cortex (DLPFC) in major depressive disorder (MDD) the fundamental neuropsychological characterization of left DLPFC hypoactivity and right DLPFC hyperactivity in MDD remains poorly understood.

We present in this paper a picture of the neural systems controlling defense that updates and simplifies Gray's "Neuropsychology of Anxiety". It is based on two behavioural dimensions: 'defensive distance' as defined by the Blanchards and 'defensive direction'. Defensive direction is a categorical dimension with avoidance of threat corresponding to fear and approach to threat corresponding to anxiety. These two psychological dimensions are mapped to underlying neural dimensions. Defensive distance is mapped to neural level, with the shortest defensive distances involving the lowest neural level (periaqueductal grey) and the largest defensive distances the highest neural level (prefrontal cortex). Defensive direction is mapped to separate parallel streams that run across these levels. A significant departure from prior models is the proposal that both fear and anxiety are represented at all levels. The theory is presented in a simplified form that does not incorporate the interactions that must occur between non-adjacent levels of the system. It also requires expansion to include the dimension of escapability of threat. Our current development and these proposed future extensions do not change the core concepts originally proposed by Gray and, we argue, demonstrate their enduring value. q

Infinitely various are the modifications of light and sound, whence they are each capable of supplying an endless variety of signs, and, accordingly, have been each employed to form languages; the one by the arbitrary appointment of mankind, the other by that of God himself. A connection established by the Author of Nature, in the ordinary course of things, may surely be called natural; as that made by men will be called artificial.

According to ''The Neuropsychology of Anxiety'' [Gray, J.A., 1982, The Neuropsychology of Anxiety: An Enquiry into the Functions of the Septo-hippocampal System, Oxford University Press, Oxford; Gray, J.A., McNaughton, N., 2000, The Neuropsychology of Anxiety: An Enquiry into the Functions of the Septo-hippocampal System, 2nd ed., Oxford University Press, Oxford], anxiolytic drugs of all types act on a behavioural inhibition system, the most important neural component of which is the septo-hippocampal system. Anxiolytics affect septo-hippocampal function by impairing the subcortical control of hippocampal 'theta' activity -the principle response of the septo-hippocampal system to arousal. Our recent experiments show that there are multiple systems controlling theta activity and that anxiolytics act on several, but not all, of these systems. This pattern of results implies that there are many different types of arousal, only some of which appear to contribute to the generation of anxiety in normal subjects and to the etiology of pathological anxiety.

The clinical characteristics of bipolar I disorder (BD1) have prognostic and therapeutic importance. The aim of this study was to examine the effect of demographic and clinical variables on the course of BD1. We reviewed the case notes of all BD1 patients (n = 63) receiving treatment in a London psychiatric service during a 1-month period. Depressive and manic onsets were equally likely without any gender difference. The earlier the age of onset, the more likely it was for patients to experience psychotic features. Only depressive onsets predicted a higher number of episodes of the same polarity. Male gender and substance abuse were associated with younger age at first presentation, while women with co-morbid substance abuse had more manic episodes. Male patients were more likely than females to be unemployed or single.

Antisocial aggression is a widespread and expensive social problem. Although aggressive behaviors and temperament are highly heritable, clinical and trait associations for the most promising candidate gene for aggression, MAOA, have been largely inconsistent. We suggest that limitations inherent to that approach might be overcome by using multimodal neuroimaging to characterize neural mechanisms of genetic risk. Herein, we detail functional, structural and connectivity findings implicating the low-expressing allele of the MAOA u-VNTR (MAOA-L) in adversely prejudicing information processing within a corticolimbic circuit composed of amygdala, rostral cingulate and medial prefrontal cortex. We propose that the MAOA-L, by causing an ontogenic excess of 5-hydroxytryptamine, labilizes critical neural circuitry for social evaluation and emotion regulation (the 'socioaffective scaffold'), thereby amplifying the effects of adverse early-life experience and creating deleterious sociocognitive biases. Our construct provides a neurobiologically consistent model for geneenvironment interactions in impulsive aggression.

Recently there has been an increase in interest in the relationship between stress and memory. Brain regions which are involved in memory function also effect the stress response. Traumatic stress results in changes in these brain regions; alterations in these brain regions in turn may mediate symptoms of posttraumatic stress disorder (PTSD). Neural mechanisms which are relevant to the effects of stress on memory, such as fear conditioning, stress sensitization, and extinction, are reviewed in relation to their implications for PTSD. Special topics including neural mechanisms in dissociation, neurobiological approaches to the validity of childhood memories as they apply to controversies over the “False Memory Syndrome,” and implications of the effects of stress on memory for psychotherapy, are also reviewed. The findings discussed in this paper are consistent with the formulation that stress-induced alterations in brain regions and systems involved in memory may underlie many of the symptoms of PTSD, as well as dissociative amnesia, seen in survivors of traumatic stress.

Borderline personality disorder (BPD) is a common disorder associated with emotional dysregulation and other symptoms that have been hypothesized to be related to dysfunction of limbic brain areas including hippocampus and amygdala. The purpose of this study was to measure hippocampal and amygdala volumes in BPD. Hippocampal and amygdala volumes were measured with magnetic resonance imaging (MRI) in 10 patients with BPD and 23 control subjects. Patients with BPD had a 21.9% smaller mean amygdala volume and a 13.1% smaller hippocampal volume, compared to controls. These findings are consistent with the hypothesis that alterations in the hippocampus and amygdala are associated with BPD. ᮊ

We are doomed to formulate conceptual structures that are much simpler than the complex phenomena they are attempting to account for. These simple conceptual structures shield us, pragmatically, from real-world complexity, but also fail, frequently, as some aspect of what we did not take into consideration makes itself manifest. The failure of our concepts dysregulates our emotions and generates anxiety, necessarily, as the unconstrained world is challenging and dangerous. Such dysregulation can turn us into rigid, totalitarian dogmatists, as we strive to maintain the structure of our no longer valid beliefs. Alternatively, we can face the underlying complexity of experience, voluntarily, gather new information, and recast and reconfigure the structures that underly our habitable worlds.

Background: Negative emotional states and abnormal stress reactivity are central components in drug addiction. The brain stress system in the amygdala is thought to play a key role in the maintenance of drug dependence through negative reinforcement. Although acute heroin administration was found to reduce anxiety, craving, and stress hormone release, whether these effects are reflected in amygdala activity has not yet been investigated.

Current Topics in Behavioral Neurosciences provides critical and comprehensive discussions of the most significant areas of behavioral neuroscience research, written by leading international authorities. Each volume offers an informative and contemporary account of its subject, making it an unrivalled reference source. Titles in this series are available in both print and electronic formats.

Background: A consistent brain activity pattern has been identified in major depression across many resting positron emission tomography (PET) studies. This dysfunctional pattern seems to be normalized by antidepressant treatment. The aim of this meta-analysis was to identify more clearly the pattern associated with clinical improvement of depression following an antidepressant drug treatment, in emotional activation studies using functional magnetic resonance imaging (fMRI). Methods: A quantitative Activation Likelihood Estimation (ALE) meta-analysis was performed across 9 emotional activation fMRI and PET studies (126 patients) using the Activation Likelihood Estimation technique. Results: Following the antidepressant drug treatment, the activation of dorsolateral, dorsomedial and ventrolateral prefrontal cortices was increased whereas the activation of the amygdala, hippocampus, parahippocampal region, ventral anterior cingulate cortex, orbitofrontal cortex, and insula was decreased. Additionally, there was a decreased activation in the anterior (BA 32) and posterior cingulate cortices, as well as in the precuneus and inferior parietal lobule, which could reflect a restored deactivation of the default mode network.

We tested the possibility suggested by previous imaging studies that amygdala participation in the storage of emotionally influenced memory is differentially lateralized in men and women. Male and female subjects received two PET scans for regional cerebral glucose-one while viewing a series of emotionally provocative (negative) films, and a second while viewing a series of matched, but emotionally more neutral, films. Consistent with suggestions from several previously published studies, enhanced activity of the right, but not the left, amygdala in men was related to enhanced memory for the emotional films. Conversely, enhanced activity of the left, but not the right, amygdala in women was related to enhanced memory for the emotional films. These results demonstrate a clear gender-related lateralization of amygdala involvement in emotionally influenced memory, and indicate that theories of the neurobiology of emotionally influenced memory must begin to account for the influence of gender. ᭧ 2001 Academic Press Converging evidence from both animal and human subject investigations strongly indicates that the amygdala is critical for enhanced explicit memory associated with emotional arousal. The evidence suggests that the amygdala interacts with endogenous stress hormones released during and after emotionally charged events to modulate memory storage occurring in other brain regions

The mirror neuron system (MNS) has been proposed to play an important role in social cognition by providing a neural mechanism by which others' actions, intentions, and emotions can be understood. Here functional magnetic resonance imaging was used to directly examine the relationship between MNS activity and two distinct indicators of social functioning in typically-developing children (aged 10.1 years ± 7 months): empathy and interpersonal competence. Reliable activity in pars opercularis, the frontal component of the MNS, was elicited by observation and imitation of emotional expressions. Importantly, activity in this region (as well as in the anterior insula and amygdala) was significantly and positively correlated with established behavioral measures indexing children's empathic behavior (during both imitation and observation) and interpersonal skills (during imitation only). These findings suggest that simulation mechanisms and the MNS may indeed be relevant to social functioning in everyday life during typical human development.

Classic minimal-group studies found that people arbitrarily assigned to a novel group quickly display a range of perceptual, affective, and behavioral in-group biases. We randomly assigned participants to a mixed-race team and used functional magnetic resonance imaging to identify brain regions involved in processing novel in-group and out-group members independently of preexisting attitudes, stereotypes, or familiarity. Whereas previous research on intergroup perception found amygdala activity-typically interpreted as negativity-in response to stigmatized social groups, we found greater activity in the amygdala, fusiform gyri, orbitofrontal cortex, and dorsal striatum when participants viewed novel in-group faces than when they viewed novel out-group faces. Moreover, activity in orbitofrontal cortex mediated the in-group bias in self-reported liking for the faces. These in-group biases in neural activity were not moderated by race or by whether participants explicitly attended to team membership or race, a finding suggesting that they occur relatively automatically. This study helps clarify the role of neural substrates involved in perceptual and affective in-group biases.

Schizophrenia and mania have a number of symptoms and epidemiological characteristics in common, and both respond to dopamine blockade. Family, twin and molecular genetic studies suggest that the reason for these similarities may be that the two conditions share certain susceptibility genes. On the other hand, individuals with schizophrenia have more obvious brain structural and neuropsychological abnormalities than those with bipolar disorder; and pre-schizophrenic children are characterised by cognitive and neuromotor impairments, which are not shared by children who later develop bipolar disorder. Furthermore, the risk-increasing effect of obstetric complications has been demonstrated for schizophrenia but not for bipolar disorder. Perinatal complications such as hypoxia are known to result in smaller volume of the amygdala and hippocampus, which have been frequently reported to be reduced in schizophrenia; familial predisposition to schizophrenia is also associated with decreased volume of these structures. We suggest a model to explain the similarities and differences between the disorders and propose that, on a background of shared genetic predisposition to psychosis, schizophrenia, but not bipolar disorder, is subject to additional genes or early insults, which impair neurodevelopment, especially of the medial temporal lobe.

Background: Previous functional brain imaging studies of social anxiety have implicated amygdala hyperactivity in response to social threat, though its relationship to quantitative measures of clinical symptomatology remains unknown. The primary aim of this study was to examine the association between response to emotionally harsh faces in the amygdala, a region implicated in social and threat-related processing, and severity of social anxiety symptoms in patients with generalized social phobia (GSP). Methods: Ten subjects with GSP naive to psychotropic medications and without psychiatric comorbidity and ten healthy comparison subjects matched on age, gender, ethnicity, and education completed the Liebowitz Social Anxiety Scale and underwent high-field (4Tesla) functional magnetic resonance imaging while viewing blocks of emotionally salient faces. Results: Relative to happy faces, activation of the amygdala in response to harsh (angry, disgusted, fearful) faces was greater in GSP patients than in controls, and the extent of amygdala activation was positively correlated with severity of social anxiety symptoms, but not general state or trait anxiety levels. Conclusions: Our findings suggest that amygdala activation to interpersonal threat can be specifically linked to the severity of social anxiety symptoms of individual GSP patients, and thus, may serve as a useful functional marker of disease severity.

SSNRIs are effective for this condition. These findings also raise the possibility that functional activity within the amygdala and VLPFC may be altered following successful treatment. Depression and Anxiety 29:328-339, 2012. C 2012 Wiley Periodicals, Inc.

Studies examining memories of arousing 'real-life' events show that emotion heightens the feeling of remembering, without necessarily enhancing the objective accuracy of the memories. We measured brain activity associated with the feeling of remembering emotional and neutral photos. Subjects indicated whether recognition was accompanied by a recollection of details about the study episode ('remember') or not ('know'). 'Remember' judgments were boosted for emotional photos, but accuracy did not differ. For neutral photos, 'remember' judgments were related to enhanced activity in the parahippocampal cortex, previously related to recognition of visual details, which one might expect to supply the retrieval clues for a 'remember' judgment. In contrast, 'remember' judgments for emotional photos were associated with enhanced activity in the amygdala, suggesting that subjects rely on arousal and perceptual fluency to evaluate these memories. For the first time, we identify the neural mechanisms underlying the enhanced feeling of remembering for emotional events.

Rarely MTS can be detected in children during the first decade of life, but is not commonly found until adolescence. Although the etiology of MTS remains controversial, there is now a considerable amount of evidence demonstrating that MTS is both a result and a cause of seizures. Clinical studies suggest that prolonged seizures or complicated febrile seizures may result in MTS. A variety of epileptogenic agents administered to adult animals have resulted in MTS and spontaneous recurrent seizures. The mechanism of the lesions is due to excessive excitability secondary to release of excitatory amino acids, primarily glutamate. Glutamate, acting at a number of subreceptors on the postsynaptic membrane, leads to prolonged depolarization of neurons and results in the entry of cytotoxic amounts of calcium. Interestingly, the same agents that produce MTS in adult animals do not produce MTS in immature animals. Clinical and experimental evidence suggests that although prolonged seizures or complicated febrile seizures can place a child at risk for MTS, a period of time is required for the lesions to develop fully.

Generalized anxiety disorder (GAD) is a prevalent anxiety disorder, but its neurobiological basis has been poorly studied. A few cognitive models have been proposed for understanding GAD development and maintenance. The aim of this study is to review functional Magnetic Resonance Image (fMRI) studies conducted with GAD patients and evaluate if they support and underpin the theoretical cognitive models proposed for this anxiety disorder. A literature systematic review was undertaken in PubMed and ISI databases with no time limits. From the studies included in this review, 10 explored the "emotional dysregulation model", showing, prefrontal cortex (PFC) and anterior cingulate cortex (ACC) hypofunction and deficient top-down control system during emotion regulation tasks, despite conflicting techniques and results. Only one study explored the "conditioned fear overgeneralization theory", other the "intolerance of uncertainty model" and two studies were uns...

The circumplex model of affect construes all emotions as linear combinations of 2 independent neurophysiological dimensions, valence and arousal. We used functional magnetic resonance imaging to identify the neural networks subserving valence and arousal, and we assessed, in 10 participants, the associations of the BOLD (blood oxygen level-dependent) response, an indirect index of neural activity, with ratings of valence and arousal during the emotional experiences induced by the presentation of evocative sentences. Unpleasant emotional experience was associated with increased BOLD signal intensities in the supplementary motor, anterior midcingulate, right dorsolateral prefrontal, occipitotemporal, inferior parietal, and cerebellar cortices. Highly arousing emotions were associated with increased BOLD signal intensities in the left thalamus, globus pallidus, caudate, parahippocampal gyrus, amygdala, premotor cortex, and cerebellar vermis. Separate analyses using a finite impulse response model confirmed these results and revealed that pleasant emotions engaged an additional network that included the midbrain, ventral striatum, and caudate nucleus, all portions of a reward circuit. These findings suggest the existence of distinct networks subserving the valence and arousal dimensions of emotions, with midline and medial temporal lobe structures mediating arousal and dorsal cortical areas and mesolimbic pathways mediating valence.

Social anxiety disorder patients suffer from excessive anxious responses in social interaction leading to avoidance behavior and social impairment. Although the amygdala has a central role in perception and processing of threatening cues, little is known about the involved networks and corresponding dysfunctions in social anxiety. Therefore, this study aims to investigate the functional connectivity network of the amygdala in patients with social anxiety disorder and to identify regions that might influence amygdalar reactivity via modulatory pathways. Ten patients with anxiety disorders (social and/or panic) and 27 healthy controls underwent a facial emotion processing task as well as 6-min functional MRI at resting state. Individual voxel-wise functional connectivity maps were calculated using the amygdala as seed region. Group comparisons were done by random-effects analysis in SPM. Patients exhibited an amygdala hyperactivation during the emotional task and decreased functional ...

Background: Generalized anxiety disorder (GAD) is a prevalent anxiety disorder, but its neurobiological basis has been poorly studied. A few cognitive models have been proposed for understanding GAD development and maintenance. The aim of this study is to review functional Magnetic Resonance Image (fMRI) studies conducted with GAD patients and evaluate if they support and underpin the theoretical cognitive models proposed for this anxiety disorder. Methods: A literature systematic review was undertaken in PubMed and ISI databases with no time limits. Results: From the studies included in this review, 10 explored the "emotional dysregulation model", showing, prefrontal cortex (PFC) and anterior cingulate cortex (ACC) hypofunction and deficient top-down control system during emotion regulation tasks, despite conflicting techniques and results. Only one study explored the "conditioned fear overgeneralization theory", other the "intolerance of uncertainty model" and two studies were unspecific (worry induction tasks). Between those, there were 4 studies evaluating pre-and posttreatment with antidepressants or "mindfulness". Limitations: The studies' methodologies differ between one another making it difficult to identify a common finding. Conclusion: Emotion dysregulation seems to be an important cognitive dysfunction in GAD patients and fMRI studies suggest that it is related to PFC and ACC hypofunction as well as a deficient cortex-amygdala functional connectivity.

Highlights

• I present an explanation of instantaneous pragmatic linguistic choice behavior.
• I posit “thin slicing” and “emotional response” behavior as mechanisms.
• My conclusion supplements other explanations based on metapragmatics and habitus.
•  I analyze examples of pragmatic choice drawn from Japanese, Persian and Javanese.

Abstract

It is axiomatic in the study of pragmatics that speakers must make choices from a myriad of variants in phonology, morphology and syntax “on the fly” during the course of interaction. However, the specific psychological and neurophysiological mechanisms that both prompt these choices have largely been taken for granted. Theoretical approaches to this problem in the past have focused on linguistic mechanisms such as “metapragmatics” or cultural approaches such as the analysis of “habitus.” While acknowledging the importance of these approaches, in this paper I extend this view by suggesting that these instantaneous choices are largely governed by the same cognitive mechanisms that govern emotional response. Drawing on the work of contemporary neurophysiology, pragmatic philosophy and phenomenology, I draw on examples from Japanese, Persian and Javanese.

Early life stress (ELS) is linked to adult psychopathology and may contribute to long-term brain alterations, as suggested by studies of women who suffered childhood sexual abuse. We examine whether reported adverse ELS defined as stressful and/or traumatic adverse childhood events (ACEs) is associated with smaller limbic and basal ganglia volumes. Method: 265 healthy Australian men and women without psychopathology or brain disorders were studied. ACEs were assessed by the ELSQ and current emotional state by the DASS. Anterior cingulate cortex (ACC), hippocampus, amygdala, and caudate nucleus volumes were measured from T1-weighted MRI. Analyses examined ROI volumetric associations with reported ACEs and DASS scores. Results: Participants with greater than two ACEs had smaller ACC and caudate nuclei than those without ACEs. A significant association between total ACEs and ROI volumes for these structures was observed. Regression analysis also revealed that ELS was more strongly associated than current emotional state (DASS) with these ROI volumes. Conclusions: Reported ELS is associated with smaller ACC and caudate volumes, but not the hippocampal or amygdala volumes. The reasons for these brain effects are not entirely clear, but may reflect the influence of early stress and traumatic events on the developing brain.

Autism and Asperger Syndrome are autism spectrum conditions (ASC) characterized by deficits in understanding others' minds, an aspect of which involves recognizing emotional expressions. This is thought to be related to atypical function and structure of the amygdala, and performance by people with ASC on emotion recognition tasks resembles that seen in people with acquired amygdala damage. In general, emotion recognition findings in ASC have been inconsistent, which may reflect low numbers of participants, low numbers of stimuli and trials, heterogeneity of symptom severity within ASC groups, and ceiling effects on some tasks. The present study tested 39 male adults with ASC and 39 typical male controls on a task of basic emotion recognition from photographs, in two separate experiments. On a control face discrimination task the group with ASC were not impaired. People with ASC were less accurate on the emotion recognition task compared to controls, but only for the negative basic emotions. This is discussed in the light of similar findings from people with damage to the amygdala.

Recent experiments investigating the effects of adrenal stress hormones on memory provide extensive evidence that epinephrine and glucocorticoids modulate long-term memory consolidation in animals and human subjects. Release of norepinephrine and activation of β-adrenoceptors within the basolateral amygdala is critical in mediating adrenal stress hormone regulation of memory consolidation. Abbreviations BLA basolateral amygdala cAMP adenosine 3′,5′-cyclic monophosphate CREB cAMP-response element-binding protein ERK2 extracellular regulated kinase GRs glucocorticoid receptors LTP long-term potentiation NCAMs neural cell adhesion molecules NMDA N-methyl-D-aspartate NTS nucleus of the solitary tract PKA cAMP-dependent protein kinase, protein kinase A

Jealousy-related behaviors such as intimate partner violence and morbid jealousy are more common in males. Principal questionnaire studies suggest that men and women have different modules to process cues of sexual and emotional infidelity. We aimed to elucidate the neural response to sentences depicting sexual and emotional infidelity in men and women using functional magnetic resonance imaging. Although there was no sex difference in the self-rating score of jealousy for sexual and emotional infidelity, men and women showed different brain activation patterns in response to the two types of infidelity. During jealous conditions, men demonstrated greater activation than women in the brain regions involved in sexual/aggressive behaviors such as the amygdala and hypothalamus. In contrast, women demonstrated greater activation in the posterior superior temporal sulcus. Our fMRI results are in favor of the notion that men and women have different neuropsychological modules to process sexual and emotional infidelity. Our findings might contribute to a better understanding of the neural basis of the jealousy-related behaviors predominantly observed in males.

In this essay I explain how classically trained voices, such as found in opera, can elicit emotional response from audience members. Key to understanding this phenomenon is understanding the nature of the "singers' formant"--a reinforced overtone in the voices of all classically trained singers that has a special neurological response in humans.

Reinforcement learning (RL) is the behavioral process of learning the values of actions and objects. Most models of RL assume that the dopaminergic prediction error signal drives plasticity in frontal–striatal circuits. The striatum then encodes value representations that drive decision processes. However, the amygdala has also been shown to play an important role in forming Pavlovian stimulus–outcome associations. These Pavlovian associations can drive motivated behavior via the amygdala projections to the ventral striatum or the ventral tegmental area. The amygdala may, therefore, play a central role in RL. Here we compare the contributions of the amygdala and the striatum to RL and show that both the amygdala and striatum learn and represent expected values in RL tasks. Furthermore, value representations in the striatum may be inherited, to some extent, from the amygdala. The striatum may, therefore, play less of a primary role in learning stimulus–outcome associations in RL than previously suggested.

A brief exploration of the ancient names for tree and almond introduces this entry. “The Semitic name for tree is Amygdala from the botanical word Amygdalus communis meaning Great Mother, archetypical Mesopotamian goddesses of life and renewal” (TL: 41, n. 9). The biblical name for tree is Luz. Prior to the Hebrew Bible, “Luz was synonymous with the old Canaanite ‘City of Almond,’ later renamed Bethel.” (TL: 41.) Relative to Bethel, both Asherah and El, essential components of Canaanite religion, were co–worshiped at Bethel/Luz.