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PubMed2005

Unilateral storage of fear memories by the amygdala.

Pavlovian fear conditioning is an associative learning task in which subjects are trained to respond defensively to a neutral conditioned stimulus (CS) by pairing it with an aversive unconditioned stimulus (US). This type of learning depends critically on the amygdala, and evidence suggests that synaptic plasticity within the lateral nucleus of the amygdala (LA) may be responsible for storing memories of the CS-US association. In the present study, we trained rats to fear an auditory CS by pairing it with a shock US delivered to one eyelid. Conditioning was assessed by measuring freezing responses evoked by the CS during a subsequent test session. The amygdala was unilaterally inactivated during either the training or the testing session by intracranial infusions of muscimol into the LA. We found that both acquisition and expression of conditioned freezing to the CS depended on the amygdala contralateral but not ipsilateral from the eyelid where the shock US was delivered. To explain this surprising result, we propose that the shock US is relayed from the eyelid to the amygdala via lateralized nociceptive sensory pathways, which causes memories of the CS-US association to be stored by the amygdala contralateral but not ipsilateral from the shocked eyelid. Our results demonstrate that the fear-learning circuitry of the amygdala is functionally lateralized according to the anatomical source of predicted threats. In future studies, the cellular mechanisms of emotional memory storage might be pinpointed by identifying cellular processes that occur only in the amygdala contralateral but not ipsilateral from the US during lateralized fear conditioning.

Acoustic Stimulation↗

PubMed2006

Stereological analysis of amygdala neuron number in autism.

The amygdala is one of several brain regions suspected to be pathological in autism. Previously, we found that young children with autism have a larger amygdala than typically developing children. Past qualitative observations of the autistic brain suggest increased cell density in some nuclei of the postmortem autistic amygdala. In this first, quantitative stereological study of the autistic brain, we counted and measured neurons in several amygdala subdivisions of 9 autism male brains and 10 age-matched male control brains. Cases with comorbid seizure disorder were excluded from the study. The amygdaloid complex was outlined on coronal sections then partitioned into five reliably defined subdivisions: (1) lateral nucleus, (2) basal nucleus, (3) accessory basal nucleus, (4) central nucleus, and (5) remaining nuclei. There is no difference in overall volume of the amygdala or in individual subdivisions. There are also no changes in cell size. However, there are significantly fewer neurons in the autistic amygdala overall and in its lateral nucleus. In conjunction with the findings from previous magnetic resonance imaging studies, the autistic amygdala appears to undergo an abnormal pattern of postnatal development that includes early enlargement and ultimately a reduced number of neurons. It will be important to determine in future studies whether neuron loss in the amygdala is a consistent characteristic of autism and whether cell loss occurs in other brain regions as well.

Adolescent↗

PubMed2004

The amygdala is enlarged in children but not adolescents with autism; the hippocampus is enlarged at all ages.

Autism is a neurodevelopmental disorder characterized by impairments in reciprocal social interaction, deficits in verbal and nonverbal communication, and a restricted repertoire of activities or interests. We performed a magnetic resonance imaging study to better define the neuropathology of autistic spectrum disorders. Here we report findings on the amygdala and the hippocampal formation. Borders of the amygdala, hippocampus, and cerebrum were defined, and their volumes were measured in male children (7.5-18.5 years of age) in four diagnostic groups: autism with mental retardation, autism without mental retardation, Asperger syndrome, and age-matched typically developing controls. Although there were no differences between groups in terms of total cerebral volume, children with autism (7.5-12.5 years of age) had larger right and left amygdala volumes than control children. There were no differences in amygdala volume between the adolescent groups (12.75-18.5 years of age). Interestingly, the amygdala in typically developing children increases substantially in volume from 7.5 to 18.5 years of age. Thus, the amygdala in children with autism is initially larger, but does not undergo the age-related increase observed in typically developing children. Children with autism, with and without mental retardation, also had a larger right hippocampal volume than typically developing controls, even after controlling for total cerebral volume. Children with autism but without mental retardation also had a larger left hippocampal volume relative to controls. These cross-sectional findings indicate an abnormal program of early amygdala development in autism and an abnormal pattern of hippocampal development that persists through adolescence. The cause of amygdala and hippocampal abnormalities in autism is currently unknown.

Adolescent↗

PubMed2005

Integrated neural representations of odor intensity and affective valence in human amygdala.

Arousal and valence are proposed to represent fundamental dimensions of emotion. The neural substrates for processing these aspects of stimuli are studied widely, with recent studies of chemosensory processing suggesting the amygdala processes intensity (a surrogate for arousal) rather than valence. However, these investigations have assumed that a valence effect in the amygdala is linear such that testing valence extremes is sufficient to infer responses across valence space. In this study, we tested an alternative hypothesis, namely that valence responses in the amygdala are nonlinear. Using event-related functional magnetic resonance imaging, we measured amygdala responses to high- and low-concentration variants of pleasant, neutral, and unpleasant odors. Our results demonstrate that the amygdala exhibits an intensity-by-valence interaction in olfactory processing. In other words, the effect of intensity on amygdala activity is not the same at all levels of valence. Specifically, the amygdala responds differentially to high (vs low)-intensity odor for pleasant and unpleasant smells but not for neutral smells. This implies that the amygdala codes neither intensity nor valence per se, but a combination that we suggest reflects the overall emotional value of a stimulus.

Adult↗

PubMed2006

Amygdala and ventromedial prefrontal cortex are inversely coupled during regulation of negative affect and predict the diurnal pattern of cortisol secretion among older adults.

Among younger adults, the ability to willfully regulate negative affect, enabling effective responses to stressful experiences, engages regions of prefrontal cortex (PFC) and the amygdala. Because regions of PFC and the amygdala are known to influence the hypothalamic-pituitary-adrenal axis, here we test whether PFC and amygdala responses during emotion regulation predict the diurnal pattern of salivary cortisol secretion. We also test whether PFC and amygdala regions are engaged during emotion regulation in older (62- to 64-year-old) rather than younger individuals. We measured brain activity using functional magnetic resonance imaging as participants regulated (increased or decreased) their affective responses or attended to negative picture stimuli. We also collected saliva samples for 1 week at home for cortisol assay. Consistent with previous work in younger samples, increasing negative affect resulted in ventral lateral, dorsolateral, and dorsomedial regions of PFC and amygdala activation. In contrast to previous work, decreasing negative affect did not produce the predicted robust pattern of higher PFC and lower amygdala activation. Individuals demonstrating the predicted effect (decrease < attend in the amygdala), however, exhibited higher signal in ventromedial prefrontal cortex (VMPFC) for the same contrast. Furthermore, participants displaying higher VMPFC and lower amygdala signal when decreasing compared with the attention control condition evidenced steeper, more normative declines in cortisol over the course of the day. Individual differences yielded the predicted link between brain function while reducing negative affect in the laboratory and diurnal regulation of endocrine activity in the home environment.

Age Factors↗

PubMed1998

Pretraining infusion of DSP-4 into the amygdala impaired retention in the inhibitory avoidance task: involvement of norepinephrine but not serotonin in memory facilitation.

The present study investigated the involvement of amygdala noradrenergic (NE) and serotonergic (5-HT) systems in memory storage processing. Rats bearing chronic cannulae in the amygdala were trained on a one-trial inhibitory avoidance task and tested for retention 24 hrs later. Five days prior to training, rats received intra-amygdala infusion of vehicle or various doses of N-2-chloroethyl-N-ethyl-2-bromobenzylamine (DSP-4)-a NE-specific neurotoxin when given peripherally. Results showed that pretraining intra-amygdala infusion of 10.0 micrograms or 30.0 micrograms of DSP-4 impaired retention. Further, 30.0 micrograms of DSP-4 also abolished the memory enhancing effect of epinephrine (E) injected peripherally. However, local infusion of DSP-4 depleted not only NE but also 5-HT and DA substantially. Subsequent experiments found that the retention deficit induced by 30.0 micrograms of DSP-4 could be ameliorated by 0.2 microgram NE but not by 5-HT at a wide range of doses infused into the amygdala shortly after training, which ascribed the deficit to depletion of NE. After protecting the 5-HT terminals by a pretreatment of fluoxetine (15.0 mg/kg), pretraining intra-amygdala infusion of 30.0 micrograms DSP-4 shifted the memory-enhancing dose of E from 0.1 mg/kg to 1.0 mg/kg. In contrast, pretraining intra-amygdala infusion of 15.0 micrograms 5,7-dihydroxytryptamine (5,7-DHT) or DSP-4 with a pretreatment of desipramine (DMI, 25.0 mg/kgx2) to protect NE terminals failed to impair retention or attenuate the memory enhancing effect of 0.1 mg/kg E injected peripherally. These findings, taken together, suggest that the memory modulatory effect of peripheral E involved, at least partially, the amygdala NE system.

5,7-Dihydroxytryptamine↗

PubMed2003

Processing of the arousal of subliminal and supraliminal emotional stimuli by the human amygdala.

The amygdala is known to play an important role in conscious and unconscious processing of emotional and highly arousing stimuli. Neuroanatomical evidence suggests that the amygdala participates in the control of autonomic responses, such as skin conductance responses (SCRs), elicited by emotionally salient stimuli, but little is known regarding its functional role in such control. We investigated this issue by showing emotional visual stimuli of varying arousal to patients with left (n = 12), right (n = 8), and bilateral (n = 3) amygdala damage and compared their results with those from 38 normal controls. Stimuli were presented both subliminally (using backward masking) and supraliminally under lateralized presentation to one visual hemifield. We collected SCRs as a physiological index of emotional responses. Subjects subsequently rated each stimulus on valence and arousal under free viewing conditions. There were two key findings: (1) impaired overall SCR after right amygdala damage; and (2) impaired correlation of SCR with the rated arousal of the stimuli after left amygdala damage. The second finding was strengthened further by finding a positive correlation between the evoked SCR magnitude and postsurgery amygdala volume, indicating impaired autonomic responses with larger tissue damage. Bilateral amygdala damage resulted in severe impairments on both of the above measures. Our results provide support for the hypothesis that the left and right amygdalae subserve different functions in emotion processing: the left may decode the arousal signaled by the specific stimulus, whereas the right may provide a global level of autonomic activation triggered automatically by any arousing stimulus.

Adult↗

PubMed1986

Effects of antidepressant drugs injected into the amygdala on behavioral responses of rats in the forced swim test.

Experiments were conducted to determine if the actions of antidepressant drugs in a pharmacological screen would be localized to specific brain regions. Rats were infused in discrete brain regions with drugs of different pharmacological properties and processed in the forced swim test. Infusion of imipramine and pargyline into the amygdala produced behavioral responses similar to i.p. injections of the drugs. The regions of the amygdala from which positive responses could be elicited were highly selective. From cannula placements and diffusion studies with autoradiography it appears that a locus of action of imipramine and pargyline is confined to the central, basolateral and/or lateral nuclear regions of the amygdala. Behavioral responses of rats in which imipramine was infused into the anterior amygdala or caudate-putamen did not differ from saline controls. When infused into regions of the amygdala in which imipramine was active, iprindole, an "atypical" antidepressant, did not produce a behavioral response in the forced swim test. Two "false positives" in the forced swim test, atropine and amphetamine, were also not active when infused into the amygdala. These results indicate that the amygdala is a critical site of action for certain antidepressant drugs in the forced swim test, and that behavioral activation in the test induced by iprindole, amphetamine and atropine involve brain regions other than the amygdala.

Amygdala↗

PubMed1974

Amygdala functions within the alimentary system.

The amygdaloid complex plays an important role in various defensive, sexual and metabolic functions of the organism. Our previous experiments on the defensive functions demonstrated that the amygdala may be divided into dorsomedial excitatory and basolateral inhibitory parts. Our recent experiments showed that this division is true also for alimentary mechanisms. The dorsomedial part of the amygdala acts as a facilitatory "center" and the lateral part as an inhibitory alimentary "center". These functions of the amygdala are parallel to those of the hypothalamic feeding centers. Bilateral damage to either the dorsomedial amygdala or to the lateral hypothalamus produced aphagia with adipsia, decrease of body weight and impairment of both classical and instrumental reactions. These changes were accompanied by low general arousal, atonia, catatonic like positions, negavitism and loss of positive emotional reactions. Damage to the lateral amygdala, on the other hand, produces a syndrome similar to damage to the ventromedial hypothalamus, i.e. hyperphagia and an increase of body weight. Slight increase of both classical and instrumental reactions and disinhibition of responses during intertrial intervals were found in both cases. Combined damage of the dorsomedial amygdala and lateral hypothalamus enhanced the symptoms attributable to each and prolonged the period of aphagia. Damage to the lateral amygdala subsequent to lesions of the dorsomedial amygdala and/or the lateral hypothalamus produced restoration of food intake, instrumental reactions and general arousal.

Amygdala↗

PubMed1993

Cholinergic drugs regulate passive avoidance performance via the amygdala.

The present study was designed to elucidate the role of the amygdala as a site of action of muscarinic and nicotinic receptor active drugs in modulating avoidance (passive avoidance) and spatial navigation (water maze) performance. Quisqualic acid lesioning of the nucleus basalis decreased choline acetyltransferase activity in the amygdala and dorsolateral frontal cortex, but not in the hippocampus. Single or combined amygdala and nucleus basalis lesions did not impair water maze navigation. Combined amygdala and nucleus basalis lesioning did not impair passive avoidance performance any more severely than did either of the lesions alone. Scopolamine (a muscarinic antagonist) and mecamylamine (a nicotinic antagonist) induced a dose-dependent impairment of both passive avoidance and water maze performance. The effects of the cholinergic antagonists on passive avoidance performance were smaller in amygdala-lesioned rats than in the controls. Amygdala lesions did not modulate the effect of the cholinergic antagonists in impairing water-maze performance. Nicotine, a nicotinic agonist, and arecoline, a muscarinic agonist, restored passive avoidance performance in nucleus basalis-lesioned but not in nucleus basalis+amygdala-lesioned rats. Nicotine and arecoline did not improve water maze navigation in nucleus basalis-lesioned or nucleus basalis+amygdala-lesioned rats. The present results suggest that the nucleus basalis cholinergic projection may modulate passive avoidance performance via amygdaloid muscarinic and nicotinic receptors.

Amygdala↗

PubMed1997

Laterality in the histological effects of injections of amyloid-beta 25-35 into the amygdala of young Fischer rats.

We have observed that single amyloid-beta 25-35 (A beta) injections (5.0 nmol) into the right amygdala of rats produce progressive cytoskeletal and astrogliotic reactions not only within the amygdala, but also in distal brain regions that project to the amygdala. To determine if these effects are potentiated by bilateral injections, we injected A beta (5.0 nmol) into the left and right amygdala of young male Fischer rats. Animals were sacrificed 32 days postoperatively. Bilateral infusions of A beta induced significant neuronal shrinkage, tau-2 neuronal staining, and reactive astrocytosis within the right amygdala and/or hippocampus, compared with vehicle-treated rats. Surprisingly, the same brain regions within the left hemisphere were significantly less affected even though no differences were observed between the left and right amygdala in the size of Congored-positive A beta deposits. Unilateral injections of A beta into the left amygdala led to significant histological changes in the right amygdala and hippocampus, but not in the same brain regions within the left hemisphere. These results suggest a laterality in the histopathological effects of A beta in male Fischer rats. Identification of the cause for the lateralized effect of A beta may prove valuable for understanding the etiology of Alzheimer disease and provide possible therapeutic strategies designed to slow the progression of the disease.

Amygdala↗

PubMed1997

Distribution of oxytocin- and vasopressin-binding sites in the rat extended amygdala: a histoautoradiographic study.

Radioligand receptor autoradiography has shown that oxytocin- and vasopressin-binding sites exist in numerous rat brain regions, among which the amygdala and the bed nucleus of the stria terminalis (BST) are especially prominent. However, these descriptions did not take into account the numerous subdivisions of the amygdala and the BST. Thus, we have reinvestigated the distribution of these sites in the rat extended amygdala, which is formed by a continuum of structures stretching from the BST to the centromedial amygdala, including parts of the accumbens nucleus, substantia innominata, and transition areas between the amygdala and the striatum. For this purpose, histoautoradiography was used to detect binding sites at the cellular level, and anatomical boundaries were defined on the basis of acetylcholinesterase histochemistry and tyrosine-hydroxylase immunohistochemistry. Oxytocin- and vasopressin-binding sites were detected in well-defined subdivisions of both medial and central parts of the extended amygdala, but they almost never coexisted in the same region. Compared with previously reported distributions, our reinvestigation describes novel oxytocin- and vasopressin-binding sites in the lateral and supracapsular BST, in the sublenticular extended amygdala, in the interstitial nucleus of the posterior limb of the anterior commissure, in the marginal zone, in the central amygdaloid nucleus, and in the anterior amygdaloid area. These results indicate that oxytocin- and vasopressin-binding sites represent an important feature of the extended amygdala and may participate in the large variety of functions that characterize this area, including reproductive and ingestive behaviors, conditioned fear and autonomic regulation.

Acetylcholinesterase↗

PubMed1997

cAMP response element-binding protein in the amygdala is required for long- but not short-term conditioned taste aversion memory.

In conditioned taste aversion (CTA) organisms learn to avoid a taste if the first encounter with that taste is followed by transient poisoning. The neural mechanisms that subserve this robust and long-lasting association of taste and malaise have not yet been elucidated, but several brain areas have been implicated in the process, including the amygdala. In this study we investigated the role of amygdala in general, and the cAMP response element-binding protein (CREB) in the amygdala in particular, in CTA learning and memory. Toward that end, we combined antisense technology in vivo with behavioral, molecular, and histochemical analysis. Local microinjection of phosphorothioate-modified oligodeoxynucleotides (ODNs) antisense to CREB into the rat amygdala several hours before CTA training transiently reduced the level of CREB protein during training and impaired CTA memory when tested 3-5 d later. In comparison, sense ODNs had no effect on memory. The effect of antisense was not attributable to differential tissue damage and was site-specific. CREB antisense in the amygdala had no effect on retrieval of CTA memory once it had been formed, and did not affect short-term CTA memory. We propose that the amygdala, specifically the central nucleus, is required for the establishment of long-term CTA memory in the behaving rat; that the process involves long-term changes, subserved by CRE-regulated gene expression, in amygdala neurons; and that the amygdala may retain some CTA-relevant information over time rather than merely modulating the gustatory trace during acquisition of CTA.

Amygdala↗

PubMed2003

Amygdala and hippocampal volumes in adolescents and adults with bipolar disorder.

BACKGROUND: The purported functions of medial temporal lobe structures suggest their involvement in the pathophysiology of bipolar disorder (BD). Previous reports of abnormalities in the volume of the amygdala and hippocampus in patients with BD have been inconsistent in their findings and limited to adult samples. Appreciation of whether volumetric abnormalities are early features of BD or whether the abnormalities represent neurodegenerative changes associated with illness duration is limited by the paucity of data in juvenile samples. OBJECTIVE: To investigate amygdala and hippocampal volume in adults and adolescents with BD. SETTING AND PARTICIPANTS: Subjects included 36 individuals (14 adolescents and 22 adults) in outpatient treatment for BD type I at a university hospital or Veterans Affairs medical center or in the surrounding community, and 56 healthy comparison subjects (23 adolescents and 33 adults). DESIGN AND MAIN OUTCOME MEASURES: Amygdala and hippocampal volumes were defined and measured on high-resolution anatomic magnetic resonance imaging scans. We used a mixed-model, repeated-measures statistical analysis to compare amygdala and hippocampal volumes across groups while covarying for total brain volume, age, and sex. Potential effects of illness features were explored, including rapid cycling, medication, alcohol or other substance dependence, duration, and mood state. RESULTS: For both the amygdala and hippocampal regions, we found an overall significant volume reduction in the BD compared with the control group (P<.0001). Amygdala volume reductions (15.6%) were highly significant (P<.0001). We observed a nonsignificant trend (P =.054) toward reductions in hippocampal volumes of lesser magnitude (5.3%). Effects of illness features were not detected. CONCLUSIONS: These results suggest that BD is associated with decreased volumes of medial temporal lobe structures, with greater effect sizes in the amygdala than in the hippocampus. These abnormalities are likely manifested early in the course of illness, as they affected adolescent and adult subjects similarly in this sample.

Adolescent↗

PubMed1988

A comparison of the efferents of the amygdala and the hippocampal formation in the rhesus monkey: I. Convergence in the entorhinal, prorhinal, and perirhinal cortices.

This is the first in a series of papers investigating the neuroanatomical basis for the interaction of the amygdala and the hippocampal formation in the rhesus monkey. The present report focuses on the complementary and convergent projections of the amygdala and hippocampal formation to the entorhinal and perirhinal cortices. These results were obtained from complementary experiments using injections of radioactively labeled amino acids to identify the anterograde projection patterns and injections of horseradish peroxidase and fluorescent retrograde tracers to confirm the cytoarchitectonic location of the neurons of origin for each projection. The results of this investigation demonstrate that both the hippocampal formation and the amygdala project to the entorhinal and perirhinal cortices where, with a few exceptions, the major projections of each structure generally are found in different layers of the same cytoarchitecture subdivisions of the entorhinal cortex but overlap in the same layers of the perirhinal cortex. Thus, the lateral and accessory basal nuclei of the amygdala project to layer 3 of areas Pr1, 28I, 28L, and 28S, and the accessory basal nucleus projects strongly to layer 1 of these same areas. In contrast, the subiculum, prosubiculum, and subfield CA1 of the of the hippocampal formation all have a projection to layer 5 of these same areas. In area 28M, the accessory basal nucleus of the amygdala projects to layer 1, while the subiculum, prosubiculum, and subfield CA1 of the hippocampal formation all project to layer 5, and the presubiculum projects to layer 3. In addition to these complementary laminar projections, there are a few areas of laminar overlap. Thus in area 28S, both the presubiculum and the CA1 subfield project to layer 3, where the lateral and accessory basal amygdaloid nuclei also project. Similarly, in 28I there is a major projection from the presubiculum and a lighter projection from the subiculum and CA1 to layer 3, where the lateral and accessory basal nuclei also project. There is also extensive laminar overlap in the perirhinal cortex. From the amygdala, the accessory basal nucleus projects to layers 1 and 3 and the lateral basal nucleus to layers 3, 5, and 6, while from the hippocampal formation, the prosubiculum projects to layers 3, 5, and 6, and the CA1 subfield projects to layer 5. This pattern of hippocampal and amygdaloid projections to the entorhinal and perirhinal cortices indicates that these cortices constitute a region of potentially extensive interaction between the amygdala and the hippocampus.

Amino Acids↗

PubMed2006

Galanin-mediated anxiolytic effect in rat central amygdala is not a result of corelease from noradrenergic terminals.

Galanin is colocalized extensively with norepinephrine in brain. Although this suggests possible activity-dependent neurotransmitter interactions, the functional significance of such colocalization remains elusive. Previously, we showed that enhancing stress-activation of the noradrenergic system by yohimbine pretreatment released galanin in central amygdala, attenuating the anxiety-like behavioral response to stress on the elevated plus-maze. The present study was conducted to determine, in this context, whether galanin was indeed coreleased from noradrenergic terminals, or instead from another galanin afferent or local stress-responsive galanin neurons in the amygdala. In experiment 1, galanin-mediated anxiolytic effects on the plus-maze following yohimbine + stress were unaltered by lesioning the noradrenergic innervation of central amygdala. In experiment 2, combining immunohistochemistry and in situ hybridization, galanin neurons specifically activated by yohimbine + stress treatment were found only in the locus coeruleus and intraamygdalar bed nucleus of the stria terminalis, adjacent to central amygdala. In experiment 3, retrograde tracing combined with in situ hybridization revealed few if any galanin cells projecting to central amygdala in locus coeruleus or nucleus tractus solitarius, sources of noradrenergic innervation. Indeed, few retrogradely-labeled galanin neurons were observed anywhere in the brain, including a small number in the intraamygdalar bed nucleus. Together, these results suggest that stress following yohimbine may have induced galanin release from an afferent to central amygdala originating in the bed nucleus, or from local neurons in the intraamygdalar bed nucleus, but that anxiolytic effects exerted by galanin in this context of elevated noradrenergic activity were not the result of corelease from noradrenergic terminals innervating central amygdala.

Adrenergic Agents↗

PubMed1999

Differential roles in the neuronal network for audiogenic seizures are observed among the inferior colliculus subnuclei and the amygdala.

The inferior colliculus (IC) is established as the initiation site within the neuronal network for audiogenic seizures (AGS), but the relative importance of the IC subnuclei in AGS is controversial. The lateral and basolateral subdivisions of the amygdala are implicated in the expansion of the AGS network that occurs during AGS kindling. However, the role of the amygdala in the AGS network in nonkindled AGS is unknown. NMDA receptors are implicated in modulation of AGS and in neurotransmission in both the IC and amygdala. Therefore, changes in AGS severity in genetically epilepsy-prone rats (GEPR-9s) were examined after bilateral focal microinjection into IC subnuclei or lateral/basolateral subdivisions of the amygdala of a competitive NMDA receptor antagonist, 3-((+)-2-carboxypiperazine-4-yl)propyl-1-phosphonic acid (CPP). Blockade of AGS in IC central nucleus (ICc) and external cortex (ICx) was observed at identical doses of CPP, but these doses were ineffective in IC dorsal cortex (ICd). Microinjection of CPP into the amygdala did not produce significant changes in AGS severity except at doses 20 times those effective in IC. The latter data contrast with the anticonvulsant effects of amygdala microinjections on seizure severity in kindled AGS reported previously. The present data in concord with neuronal recording studies of these nuclei suggest that the ICc is the most critical site in AGS initiation, the ICx in propagation, and that the ICd plays a lesser role in the AGS network. The amygdala does not appear to play a requisite role in the neuronal network for AGS in animals that have not been subjected to AGS kindling.

Acoustic Stimulation↗

PubMed2002

The amygdala response to emotional stimuli: a comparison of faces and scenes.

As a central fear processor of the brain, the amygdala initiates a cascade of critical physiological and behavioral responses. Neuroimaging studies have shown that the human amygdala responds not only to fearful and angry facial expressions but also to fearful and threatening scenes such as attacks, explosions, and mutilations. Given the relative importance of facial expressions in adaptive social behavior, we hypothesized that the human amygdala would exhibit a stronger response to angry and fearful facial expressions in comparison to other fearful and threatening stimuli. Twelve subjects completed two tasks while undergoing fMRI: matching angry or fearful facial expressions, and matching scenes depicting fearful or threatening situations derived from the International Affective Picture System (IAPS). While there was an amygdala response to both facial expressions and IAPS stimuli, direct comparison revealed that the amygdala response to facial expressions was significantly greater than that to IAPS stimuli. Autonomic reactivity, measured by skin conductance responses, was also greater to facial expressions. These results suggest that the human amygdala shows a stronger response to affective facial expressions than to scenes, a bias that should be considered in the design of experimental paradigms interested in probing amygdala function.

Adult↗