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PubMed2002

Ecstasy and agony: activation of the human amygdala in positive and negative emotion.

Considerable evidence indicates that the amygdala plays a critical role in negative, aversive human emotions. Although researchers have speculated that the amygdala plays a role in positive emotion, little relevant evidence exists. We examined the neural correlates of positive and negative emotion using positron emission tomography (PET), focusing on the amygdala. Participants viewed positive and negative photographs, as well as interesting and uninteresting neutral photographs, during PET scanning. The left amygdala and ventromedial prefrontal cortex were activated during positive emotion, and bilateral amygdala activation occurred during negative emotion. High-interest, unusual photographs also elicited left-amygdala activation, a finding consistent with suggestions that the amygdala is involved in vigilance reactions to associatively ambiguous stimuli. The current results constitute the first neuroimaging evidence for a role of the amygdala in positive emotional reactions elicited by visual stimuli. Although the amygdala appears to play a more extensive role in negative emotion, it is involved in positive emotion as well.

Adult↗
PubMed2004

Impaired judgments of sadness but not happiness following bilateral amygdala damage.

Although the amygdala's role in processing facial expressions of fear has been well established, its role in the processing of other emotions is unclear. In particular, evidence for the amygdala's involvement in processing expressions of happiness and sadness remains controversial. To clarify this issue, we constructed a series of morphed stimuli whose emotional expression varied gradually from very faint to more pronounced. Five morphs each of sadness and happiness, as well as neutral faces, were shown to 27 subjects with unilateral amygdala damage and 5 with complete bilateral amygdala damage, whose data were compared to those from 12 brain damaged and 26 normal controls. Subjects were asked to rate the intensity and to label the stimuli. Subjects with unilateral amygdala damage performed very comparably to controls. By contrast, subjects with bilateral amygdala damage showed a specific impairment in rating sad faces, but performed normally in rating happy faces. Furthermore, subjects with right unilateral amygdala damage performed somewhat worse than subjects with left unilateral amygdala damage. The findings suggest that the amygdala's role in processing of emotional facial expressions encompasses multiple negatively valenced emotions, including fear and sadness.

Amygdala↗
PubMed2004

The amygdala and persistent pain.

A reciprocal relationship exists between persistent pain and negative affective states such as fear, anxiety, and depression. Accumulating evidence points to the amygdala as an important site of such interaction. Whereas a key role of the amygdala in the neuronal mechanisms of emotionality and affective disorders has been well established, the concept of the amygdala as an important contributor to pain and its emotional component is still emerging. This article will review and discuss evidence from anatomical, neuroimaging, behavioral, electrophysiological, pharmacological, and biochemical data that implicate the amygdala in pain modulation and emotional responses to pain. The latero-capsular division of the central nucleus of the amygdala is now defined as the "nociceptive amygdala" and integrates nociceptive information with poly-modal information about the internal and external bodily environment. Dependent on environmental conditions and affective states, the amygdala appears to play a dual facilitatory and inhibitory role in the modulation of pain behavior and nociceptive processing at different levels of the pain neuraxis. Only recently, electrophysiological, pharmacological, and biochemical neuroplastic changes were shown in the nociceptive amygdala in persistent pain. It is conceivable, however, that amygdala plasticity plays an important role in emotional pain behavior and its modulation by affective state.

Amygdala↗
PubMed2006

Measurements of the amygdala and hippocampus in pathologically confirmed Alzheimer disease and frontotemporal lobar degeneration.

BACKGROUND: Differentiating between Alzheimer disease (AD) and frontotemporal lobar degeneration (FTLD) can be difficult, particularly in the earliest stages of the diseases. Patterns of atrophy on magnetic resonance imaging may help distinguish these diseases and aid diagnosis. OBJECTIVE: To assess the diagnostic utility of magnetic resonance imaging-derived amygdala and hippocampal volumes from patients with pathologically proved AD and FTLD. DESIGN: Cross-sectional volumetric magnetic resonance imaging study of the hippocampus and amygdala. SETTING: Specialist cognitive disorders clinic. Subjects Thirty-seven subjects, including 10 patients with pathologically proved AD, 17 patients with pathologically proved FTLD, and 10 age-matched control subjects. MAIN OUTCOME MEASURES: Hippocampal and amygdala volumes. RESULTS: Geometric mean amygdala and hippocampal volumes were, respectively, 15.0% (95% confidence interval [CI], 4.2%-24.5%) and 16.4% (95% CI, 5.9%-25.6%) lower in the AD than in the control group. In FTLD, the equivalent differences were 43.1% (95% CI, 31.9%-52.6%) in the amygdala and 36.1% (95% CI, 27.5%-43.7%) in the hippocampus. Volumes were significantly lower in the FTLD than in the AD group (P<.01 in both regions). Within the FTLD clinical subgroups, there was evidence of a difference in pattern of atrophy with greater asymmetry (left smaller than right) in semantic dementia compared with frontal variant FTLD (P<.001). On average, the left hippocampus was 14% smaller in semantic dementia than in frontal variant FTLD, whereas the right hippocampus was 37% larger. On average, the left amygdala was 39% smaller in semantic dementia than in frontal variant FTLD, whereas the right amygdala was only 1% smaller. CONCLUSIONS: Hippocampal atrophy is not specific to AD or FTLD. However, severe or asymmetrical amygdala atrophy should suggest FTLD. Atrophy patterns follow clinical syndromes rather than pathology.

Adult↗
PubMed2005

A susceptibility gene for affective disorders and the response of the human amygdala.

BACKGROUND: A common regulatory variant (5-HTTLPR) in the human serotonin transporter gene (SLC6A4), resulting in altered transcription and transporter availability, has been associated with vulnerability for affective disorders, including anxiety and depression. A recent functional magnetic resonance imaging study suggested that this association may be mediated by 5-HTTLPR effects on the response bias of the human amygdala-a brain region critical for emotional and social behavior-to environmental threat. OBJECTIVES AND DESIGN: To examine the effects of 5-HTTLPR genotype on the reactivity of the human amygdala to salient environmental cues with functional magnetic resonance imaging in a large (N = 92) cohort of volunteers carefully screened for past and present medical or psychiatric illness, and to explore the effects of 5-HTTLPR genotype as well as amygdala reactivity on harm avoidance, a putative personality measure related to trait anxiety. RESULTS: We now confirm the finding of 5-HTTLPR short allele-driven amygdala hyperreactivity in a large independent cohort of healthy subjects with no history of psychiatric illness or treatment. Furthermore, we demonstrate that these genotype effects on amygdala function are consistent with a dominant short allele effect and are equally prominent in men and women. However, neither 5-HTTLPR genotype, amygdala reactivity, nor genotype-driven variability in this reactivity was reflected in harm avoidance scores. CONCLUSIONS: Our results reveal a potent modulatory effect of the 5-HTTLPR on amygdala reactivity to environmental threat. Since this genetically driven effect exists in healthy subjects, it does not, in and of itself, predict dimensions of mood or temperament. As such, the 5-HTTLPR may represent a classic susceptibility factor for affective disorders by biasing the functional reactivity of the human amygdala in the context of stressful life experiences and/or deficient cortical regulatory input.

Adult↗
PubMed2006

Amygdala-prefrontal dissociation of subliminal and supraliminal fear.

Facial expressions of fear are universally recognized signals of potential threat. Humans may have evolved specialized neural systems for responding to fear in the absence of conscious stimulus detection. We used functional neuroimaging to establish whether the amygdala and the medial prefrontal regions to which it projects are engaged by subliminal fearful faces and whether responses to subliminal fear are distinguished from those to supraliminal fear. We also examined the time course of amygdala-medial prefrontal responses to supraliminal and subliminal fear. Stimuli were fearful and neutral baseline faces, presented under subliminal (16.7 ms and masked) or supraliminal (500 ms) conditions. Skin conductance responses (SCRs) were recorded simultaneously as an objective index of fear perception. SPM2 was used to undertake search region-of-interest (ROI) analyses for the amygdala and medial prefrontal (including anterior cingulate) cortex, and complementary whole-brain analyses. Time series data were extracted from ROIs to examine activity across early versus late phases of the experiment. SCRs and amygdala activity were enhanced in response to both subliminal and supraliminal fear perception. Time series analysis showed a trend toward greater right amygdala responses to subliminal fear, but left-sided responses to supraliminal fear. Cortically, subliminal fear was distinguished by right ventral anterior cingulate activity and supraliminal fear by dorsal anterior cingulate and medial prefrontal activity. Although subcortical amygdala activity was relatively persistent for subliminal fear, supraliminal fear showed more sustained cortical activity. The findings suggest that preverbal processing of fear may occur via a direct rostral-ventral amygdala pathway without the need for conscious surveillance, whereas elaboration of consciously attended signals of fear may rely on higher-order processing within a dorsal cortico-amygdala pathway.

Adult↗
PubMed2002

Human amygdala responses to fearful eyes.

Fearful facial expressions evoke increased neural responses in human amygdala. We used event-related fMRI to investigate whether eye or mouth components of a fearful face are critical in evoking this increased amygdala activity. In addition to prototypical fearful (FF) and neutral (NN) faces, subjects viewed two types of chimerical face: fearful eyes combined with a neutral mouth (FN), and neutral eyes combined with a fearful mouth (NF). FE faces evoked specific responses in left anterior amygdala. FN faces evoked responses in bilateral posterior amygdala and superior colliculus. Responses in right amygdala, superior colliculus, and pulvinar exhibited significant time x condition interactions with respect to faces with fearful eyes (FF, FN) vs neutral eyes (NF, NN). These data indicate that fearful eyes alone are sufficient to evoke increased amygdala activity. In addition, however, left amygdala displayed discriminatory responses to fearful eyes in different configural contexts (i.e., in FF and FN faces). These results suggest, therefore, that human amygdala responds to both feature-specific and configural aspects of fearful facial expressions.

Adult↗
PubMed2001

Amygdala, hippocampus, and unconditioned fear.

Embedded within contemporary views of emotional learning is a well-founded agreement that the amygdala plays a pivotal role in the formation and consolidation of aversive memories formed during fear conditioning. However, it is important to determine whether observed deficits are reflective of a memory impairment or whether they are simply attributable to a deficit in the performance of unconditioned fear responses such as freezing. Within the neurobiology of learning and memory literature, there is an ongoing debate concerning the potential role of the amygdala in the performance of unconditioned fear responses. A view put forth by Vazdarjanova and McGaugh (1998) suggests that the amygdala is not required for the formation and consolidation of the aversive memories formed during fear conditioning, but is essential in the performance of unconditioned fear responses. Data provided by Maren (1999) counter this view by positing that the amygdala is not required for the performance of fear responses, but its role is of a mnemonic nature in the conditioning of fear to neutral cues. To clarify the amygdala's participation in these two processes, a useful approach would involve a situation where animals with amygdala damage were examined for their unconditioned fear responses in reaction to footshock as well as the conditioning of these reactions to previously neutral cues paired with the aversive event. We have previously reported that rats with amygdala or hippocampal damage are impaired in discriminative fear conditioning to context. In the present experiment, we report the initial unconditioned fear responses to footshock by these same animals as well as the conditioned responses during testing. In both groups, the fear responses assessed (freezing, urination, defecation, and locomotion) were not impaired and did not differ from those expressed by the sham animals. The impairment of discriminative fear conditioning to context, in combination with the present experiment, represents a dissociation where damage to specific memory structures (amygdala or hippocampus) debilitates the mnemonic processes involved in fear conditioning, but not the performance of the fear responses per se.

Amygdala↗
PubMed1998

Aspiration lesions of the amygdala disrupt the rhinal corticothalamic projection system in rhesus monkeys.

In macaque monkeys, aspiration but not excitotoxic lesions of the medial temporal lobe limbic structures, the amygdala and hippocampus, produce a severe impairment in visual recognition memory. Furthermore, certain ventromedial cortical regions, namely the rhinal (i.e., entorhinal and perirhinal) cortex, are now known to be critical for visual recognition memory. Because the route taken by temporal cortical efferent fibers, especially perirhinal efferents, passes nearby the amygdala, it is possible that inadvertent damage to these fibers is produced by the aspirative but not the excitotoxic process, thereby accounting at least in part for the different behavioral outcomes of the two types of lesion. To test this idea, we assessed the integrity of the rhinal corticothalamic projection system after aspiration lesions of the amygdala. Three rhesus monkeys with unilateral amygdala removals received bilaterally symmetrical injections of a retrograde fluorescent tracer into the medial portion of the mediodorsal nucleus of the thalamus. Retrogradely labeled cells were identified using conventional fluorescence microscopy techniques. In all three cases, the rhinal cortex of the intact hemispheres contained moderate numbers of retrogradely labeled cells. By contrast, the rhinal cortex of the amygdalectomized hemispheres consistently contained few retrogradely labeled cells, and a direct comparison of the two hemispheres showed this difference to be statistically significant. A similar asymmetric pattern was observed for area TE but not for the cortex lining the dorsal bank of the superior temporal sulcus, nor for the rostral cingulate motor area, which was examined as a control. The results indicate that aspiration lesions of the amygdala not only remove the cell bodies of the amygdala, as intended, but also inadvertently disrupt projection fibers arising from cells in the rhinal cortex and area TE that pass nearby or through the amygdala en route to the thalamus. Behavioral studies examining the effects of aspiration lesions of the amygdala in nonhuman primates need to take these findings into consideration.

Amygdala↗
PubMed2006

Reduction of apoptosis in the amygdala by an A2A adenosine receptor agonist following myocardial infarction.

It has been observed that a cytokine synthesis inhibitor, pentoxifylline, prevents the apoptotic processes taking place in the amygdala following myocardial infarction. However, it is unknown if the cardioprotective effect of A(2A) adenosine receptor agonist, CGS21680, which reduces cytokine synthesis, would lead to such amygdala apoptosis regression. Thus, this study was designed to investigate whether cardioprotective A(2A) adenosine receptor activation reduces apoptosis in the amygdala following myocardial infarction. Anesthetized rats were subjected to left anterior descending coronary artery occlusion for 40 min, followed by 72 h of reperfusion. The A(2A) agonist CGS21680 (0.2 mug/kg/min i.v.) was administered continuously for 120 min, starting (1) five minutes prior to instituting reperfusion (Early) or (2) five minutes after the beginning of reperfusion (Late). After reperfusion, myocardial infarct size was determined and the amygdala was dissected from the brain. Infarct size was reduced significantly in the Early compared to the Control group (34.6 +/- 1.8% and 52.3 +/- 2.8% respectively; p < 0.05), with no difference compared to the Late group (40.1 +/- 6.1%). Apoptosis regression was documented in the amygdala of the Early group by an enhanced phosphatidylinositol 3-kinase-Akt pathway activation and Bcl-2 expression concurrently to a caspase-3 activation limitation and reduction in TUNEL-positive cells staining. On the other hand, amygdala TUNEL-positive cell numbers were not reduced in the Late group. Moreover, TNFalpha was significantly reduced in the amygdala of the Early group compared to the Control and Late groups. These results indicate that A(2A) adenosine receptor stimulation is associated with apoptosis regression in the amygdala following myocardial infarction.

Adenosine↗
PubMed1976

Impaired retention of visual discriminated escape training produced by subseizure amygdala stimulation.

These experiments examined the effects on memory of posttrial, subseizure, electrical stimulation of the amygdala. Rats were trained in a visual discriminated avoidance Y-maze. Each animal received 6 tirals on the training day. Retention, tested the following day, was measured both by the number of correct choices on the first 6 retraining trials and by the number of trials to a criterion of 5 of 6 correct choices. If administered 2 min, 1 h, or 4 h, but not 10 h, after training, bilateral amygdala stimulation significantly impaired retention as measured 24 h after training. In a second experiment, rats received unilateral amygdala stimulation in order to examine better the anatomical localization of effective stimulation sites. The unilateral stimulation was administered either 2 min, 10 min, 1 h, or 4 h after training. The behavioral procedures were the same as those used in the first experiment. For animals stimulated 2 min after training, the optimal stimulation region was one which extended rostrally from the ventrolateral portion of the basomedial nucleus to the dorsomedial region of the amygdala near the stria terminalis and nucleus centralis. For animals stimulated after a 10 min training-treatment interval, this amygdala region was not an effective stimulation site. However, in these animals, stimulation of the basolateral nucleus impaired later retention. Unilateral, posttraining amygdala stimulation administered 1 or 4 h after training did not appear to produce retention deficits. The findings of these experiments thus indicate that posttrial unilateral or bilateral amygdala stimulation impairs retention of discriminated avoidance training. Furthermore, the specific amygdala site at which posttrial stimulation impairs later retention varies with the training-treatment interval.

Amygdala↗
PubMed1977

Amygdala afferents from the mediobasal hypothalamus: an electrophysiological and neuroanatomical study in the rat.

Electrophysiological techniques and the retrograde transport of horseradish peroxidase (HRP) were used to determine the efferent projections from the caudal mediobasal hypothalamus to the amygdala. In pentobarbital anesthetized rats, the activity of 1780 mediobasal hypothalamic neurons was examined for response to stimulation sites in the amygdala and stria terminalis. Evidence of orthodromic activation from both stimulation sties was commonly observed. Sixty-five cells mostly located in the ventromedial nucleus displayed antidromic invasion from the basolateral, basomedial or cortical amygdala over a latency range of 5-34 msec (mean 15.3 +/- 6.7 msec S.D.). Three of 440 tested cells displayed antidromic activation from stimulation on the stria terminalis. Amygdala evoked antidromic responses were still present after lesions of the stria terminalis. May ipsilateral ventromedial hypothalamic neurons and a few cells in the ipsilateral arcuate nucelus and periventricular region and contralateral ventromedial nucleus displayed retrograde transport of HRP after an infection into the amygdala. Lesions of the stria terminalis had little effect on the numbers of HRP labeled neurons. Relatively more neurons were labeled retrogradely after medial injections than after lateral injections in the amygdala. Data from both electrophysiological and anatomical techniques therefore indicate that certain mediobasal hypothalamic neurons, particularly those located in the ipsilateral ventromedial nucleus, project to the amygdala probably via a route other than the stria terminalis. Thus there is substantial evidence in the rat for reciprocal connections between the amygdala and the hypothalamic ventromedial nucleus.

Afferent Pathways↗
PubMed1977

Modulation of the proestrous surge of luteinizing hormone by electrochemical stimulation of the amygdala and hippocampus in the unanesthetized rat.

The roles played by the amygdala and hippocampus in controlling the release of pituitary luteinizing hormone (LH) were studied in the freely moving rat. Monopolar stainless steel electrodes were implanted into the corticomedial (CM) amygdala, basolateral (BL) amygdala and dorsal hippocampus of female rats. When the animal had recovered from surgery and shown two consecutive 4-day estrous cycles, a chronic atrial cannula was introduced during the afternoon of diestrus II. On the following day (proestrus) electrochemical stimulation (ECS) was applied (20--50 micronA anodal DC 120 sec) bilaterally to the amygdala or hippocampus and blood samples were taken every 90 min from 12.00 to 21.00 h for radioimmunoassay (RIA) of LH. Next day, uterine tubes were examined for ova as evidence of ovulation. ECS of the amygdala exerted two divergent influences on LH release. Stimulation of the BL amygdala at 13.45 h, just before the critical period (14.00--16.00 h), was effective in delaying and reducing the LH surge, whereas ECS of the CM amygdala at 12.00 h resulted in an early synchronization in the timing of the LH curves. All of the rats in both groups ovulated, in contrast to the results of applying ECS to the dorsal hippocampus; there the LH surge and ovulation were completely blocked in 7 out of 9 rats. Thus, in the freely moving rat, the hippocampus can exert a potent inhibitory influence on LH release whereas the amygdala plays a modulatory role in the process.

Amygdala↗
PubMed1988

The effects of various lesions and knife-cuts on septal and amygdala kindling in the rat.

Large bilateral aspiration lesions of the hippocampus had no significant effect on septal kindling, whereas large bilateral DC lesions of the pyriform lobe resulted in a small but significant increase in the number of septal stimulations required to complete kindling. Bilateral aspiration lesions of the dorsal hippocampus or large bilateral DC lesions of the ventral hippocampus had no effect on amygdala kindling. Small DC lesions of the stria terminalis significantly facilitated amygdala kindling. Unilateral or bilateral ventral knife-cuts delivered in a coronal plane anterior to the amygdala, disrupting communication with anterior pyriform structures, produced a small but nearly significant increase in the number of stimulations required for amygdala kindling. Similar cuts placed posterior to the amygdala, disrupting communication with the hippocampus, significantly facilitated kindling. Cuts that were medially placed, to disrupt the ventral amygdala-fugal pathway, had no effect on amygdala kindling. These results show that the hippocampus is not critical for either septal or amygdala kindling. The pyriform lobe structures appear to play a facilitatory role in kindling, but none of the lesions or knife-cuts were capable of blocking or even severely retarding kindling.

Amygdala↗
PubMed1994

Attenuated hippocampal long-term potentiation in basolateral amygdala-lesioned rats.

Possible involvement of the amygdaloid input in long-term potentiation (LTP) in the medial perforant path-dentate gyrus granule cell synapses in vivo was investigated by evaluating the effects of lesions of the amygdaloid nucleus. The dentate gyrus synaptic potential evoked by low-frequency test stimulation did not change following lesions of the basolateral and central amygdala. However, when tetanic stimulation (30 pulses at 60 Hz) was applied 60 min after lesioning of the ipsilateral basolateral amygdala, the magnitude of LTP was significantly attenuated. Since lesions of the ipsilateral central amygdala and the contralateral basolateral amygdala did not affect the dentate gyrus LTP, the attenuation of the dentate gyrus LTP is a specific effect of acute lesions of the ipsilateral basolateral amygdala. The basolateral amygdaloid lesions significantly attenuated both LTP induced by weak (20 pulses at 60 Hz) and strong (100 pulses at 100 Hz) tetanus, indicating that the effect of the lesions does not depend on the strength of tetanus applied to induce LTP. When the ipsilateral basolateral amygdala was destroyed after application of tetanus, it did not affect the established LTP. The attenuation of LTP was also observed after the basolateral amygdala-lesioned rats were allowed a recovery period of 2 weeks. This is the first report providing evidence that the ipsilateral basolateral amygdala modulates hippocampal synaptic plasticity in vivo.

Amygdala↗
PubMed1996

Medial amygdaloid suppression of predatory attack behavior in the cat: I Role of a substance P pathway from the medial amygdala to the medial hypothalamus.

The medial amygdala is known to powerfully suppress predatory attack behavior in the cat, but the mechanisms underlying such modulation remain unknown. The present study tested the hypothesis that medial amygdaloid suppression of predatory attack is mediated, in part, by a pathway from the medial amygdala to the medial hypothalamus which utilizes substance P as a neurotransmitter. Stimulating electrodes were implanted into the medial amygdala and cannula electrodes were implanted into both the medial and lateral hypothalamus. Predatory attack behavior was elicited by electrical stimulation of the lateral hypothalamus. In the first phase of the study, paired trials compared attack latencies of single stimulation of the lateral hypothalamus with those following dual stimulation of the lateral hypothalamus and medial amygdala. Attack latencies were significantly elevated following dual stimulation of the medial amygdala and lateral hypothalamus. In the second phase of the study, dose and time dependent decreases in response suppression were noted following the infusion of the substance P (NK1) receptor antagonist, CP96.345 (in doses of 0.05, 0.5 and 2.5 nmol) into the medial hypothalamus. In third phase of the study, the effects of microinjections of the substance P receptor agonist, [Sar9.Met(O2)11]-substance P (in doses of 0.5, 1.0 and 2.0 nmol), directly into the medial hypothalamus upon lateral hypothalamically elicited predatory attack behavior were determined. Microinfusion of this drug elevated attack response latencies in a dose- and time-dependent manner. In addition, pretreatment with CP96,345 into the medial hypothalamus blocked the suppressive effects of subsequent delivery of [Sar9,Met(O2)11]-substance P into the same medial hypothalamic site. Other parts of the study demonstrated the presence of: (1) high densities of substance P receptors in the ventromedial hypothalamus, and (2) neurons that are positively labeled for substance P that project from the medial amygdala to the ventromedial hypothalamus as demonstrated by retrograde labeling with Fluoro-Gold. These findings provide support for the hypothesis that medial amygdaloid suppression of lateral hypothalamically elicited predatory attack behavior includes a substance P pathway from the medial amygdala to the medial hypothalamus. The findings further suggest that stimulation of the medial amygdala activates substance P receptors in the medial hypothalamus, thus triggering an inhibitory mechanism from the medial to the lateral hypothalamus, resulting in suppression of predatory attack behavior.

Amygdala↗
PubMed1986

Deep prepyriform cortex kindling and its relation to amygdala kindling in the rat.

Kindling of the deep prepyriform cortex (DPC), a recently identified sensitive site to chemoconvulsants, was compared to kindling of the amygdala in rats. Although the two kindled sites were very similar in their initial responses, electroencephalographic changes during kindling stimulation, kindling seizure development, and growth of afterdischarge, they differed in that the deep prepyriform cortex showed a significantly lower final threshold, a significantly higher frequency of afterdischarge and a significantly shorter latency to bilateral forelimb clonus than the amygdala. Significant bidirectional transfer was found during secondary kindling of either of the two sites, suggesting a close interrelation between them. Rhythmic synchronous discharge was directly induced in the deep prepyriform cortex by ipsilateral amygdala stimulation, but not in the amygdala by ipsilateral cortical stimulation. Local application of both muscimol (0.45 nM) and 2-amino-5-phosphonovaleric acid (25 nM) into the cortical site reduced the afterdischarge duration of amygdala-kindled seizures by approximately 20% without changing the type or duration of the motor seizure. We suggest that the deep prepyriform cortex is "downstream" from the amygdala in the preferential routes of afterdischarge propagation, and that, although the deep prepyriform cortical neurocircuits of GABA and excitatory amino acids may be involved in the maintenance of amygdala-kindled, self-sustained afterdischarge, they are not essential in the expression of amygdala-kindled motor convulsions.

2-Amino-5-phosphonovalerate↗
PubMed1988

Amygdala kindling and c-fos protein(s).

c-fos protein was visualized immunohistochemically in the brains of rats after partial amygdala seizures and generalized amygdala-kindled seizures and in seizure-free amygdala-kindled rats. Four hours following partial amygdala seizures there was a massive induction of c-fos protein in the ipsilateral piriform cortex, entorhinal cortex, and amygdala. Following generalized amygdala-kindled seizures there was a massive bilateral induction of c-fos in the entire cerebral cortex, amygdala, piriform and entorhinal cortices, hippocampus, and dentate gyrus. However, there did not appear to be any change in the basal levels of c-fos in the brains of amygdala-kindled rats that had been seizure free for 7 days. These results show that kindled seizures induce c-fos in neurons, but that the permanence of kindling is not related to altered basal c-fos levels.

Amygdala↗