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At least 19 recordsLinked to original sources
PubMed2005

Subpallial amygdala and nucleus taeniae in birds resemble extended amygdala and medial amygdala in mammals in their expression of markers of regional identity.

Two regions were recently recognized as subpallial amygdaloid nuclei in birds, the nucleus taeniae of the amygdala (TnA) and the newly identified subpallial amygdala (SpA). Here we further confirm these nuclei to be subpallial and amygdaloid and show similarity to specific mammalian subpallial amygdaloid nuclei. By its topological, connectional and neurochemical traits, avian TnA has been suggested to be comparable to mammalian medial amygdala (MeA) and SpA to be comparable to the sublenticular part of mammalian extended amygdala (ExA). We examined molecular traits of these areas using immunohistochemistry for limbic system-associated membrane protein (LAMP) and in situ hybridization for glutamic acid decarboxylase-65 (GAD65) and chicken ovalbumin upstream promoter-transcription factor II (COUP-TF II). Mammalian GAD65 is a subpallial marker and was enriched in ExA and MeA. Chick GAD65 was enriched in SpA and TnA, indicating that they are subpallial. LAMP, which is enriched in limbic regions such as mammalian ExA and MeA, was enriched in avian SpA and TnA. COUP-TF II was enriched in mammalian amygdala including MeA and ExA to a lesser extent. In birds, COUP-TF II was enriched in TnA and moderate in SpA. Overlap of these markers confirms avian TnA resembles mammalian MeA and SpA resembles ExA.

Amygdala↗
PubMed2002

Is the human amygdala critical for the subjective experience of emotion? Evidence of intact dispositional affect in patients with amygdala lesions.

It is thought that the human amygdala is a critical component of the neural substrates of emotional experience, involved particularly in the generation of fear, anxiety, and general negative affectivity. Although many neuroimaging studies demonstrate findings consistent this notion, little evidence of altered emotional experience following amygdala damage has been gathered in humans. In a preliminary test of the amygdala's role in phenomenal affective states, we assessed the extent of experienced positive and negative affective states in patients with amygdala damage and age-, sex-, and education-matched controls. To assess chronic changes in experienced affect, all groups were administered the Positive and Negative Affect Schedules (PANAS, Watson, Clark, & Tellegen, 1988). In the first study, we examined the effects of amygdala lesions on affective traits in 10 left and 10 right amygdala-damaged patients, 1 patient with bilateral amygdala damage (SP), and 20 control subjects. Subjects were asked to indicate the typicality of different experiential states of positive (e.g., inspired, excited) and negative (e.g., afraid, nervous) valence. In a second study, we examined more closely the effects of bilateral amygdala damage on the day-to-day generation of affective states by administering the PANAS daily for a 30-day period to patient SP and age-, sex-, and education-matched controls. In both experiments, no differences in the magnitude and frequency of self-reported positive or negative affect were found between control subjects and patients with amygdala damage. Moreover, principal components analyses of the covariation among different affects (across individuals in Study 1 and within individuals across days in Study 2) confirmed a two-factor (positive vs. negative) description of experienced affect in controls. A highly similar two-factor description of experienced affect was found in patients with amygdala lesions. This suggests that the underlying structure of affective states was intact following amygdala damage. It is concluded that the human amygdala may be recruited during phenomenal affective states in the intact brain, but is not necessary for the production of these states.

Adult↗
PubMed2001

Functional and anatomical localization of mu opioid receptors in the striatum, amygdala, and extended amygdala of the nonhuman primate.

The subregional distribution of mu opioid receptors and corresponding G-protein activation were examined in the striatum, amygdala, and extended amygdala of cynomolgus monkeys. The topography of mu binding sites was defined using autoradiography with [(3)H]DAMGO, a selective mu ligand. In adjacent sections, the distribution of receptor-activated G proteins was identified with DAMGO-stimulated guanylyl 5'(gamma-[(35)S]thio)triphosphate ([(35)S]GTPgammaS) binding. Within the striatum, the distribution of [(3)H]DAMGO binding sites was characterized by a distinct dorsal-ventral gradient with a higher concentration of binding sites at more rostral levels of the striatum. [(3)H]DAMGO binding was further distinguished by the presence of patch-like aggregations within the caudate, as well as smaller areas of very dense receptor binding sites, previously identified in human striatum as neurochemically unique domains of the accumbens and putamen (NUDAPs). The amygdala contained the highest concentration of [(3)H]DAMGO binding sites measured in this study, with the densest levels of binding noted within the basal, accessory basal, paralaminar, and medial nuclei. In the striatum and amygdala, the distribution of DAMGO-stimulated G-protein activation largely corresponded with the distribution of mu binding sites. The central and medial nuclei of the amygdala, however, were notable exceptions. Whereas the concentration of [(3)H]DAMGO binding sites in the central nucleus of the amygdala was very low, the concentration of DAMGO-stimulated G-protein activation in this nucleus, as measured with [(35)S]GTPgammaS binding, was relatively high compared to other portions of the amygdala containing much higher concentrations of [(3)H]DAMGO binding sites. The converse was true in the medial nucleus, where high concentrations of binding sites were associated with lower levels of DAMGO-stimulated G-protein activation. Finally, [(3)H]DAMGO and [(35)S]GTPgammaS binding within the amygdala, particularly the medial nucleus, formed a continuum with the substantia innominata and bed nucleus of the stria terminalis, supporting the concept of the extended amygdala in primates.

Amygdala↗
PubMed1992

Equipotentiality of thalamo-amygdala and thalamo-cortico-amygdala circuits in auditory fear conditioning.

The goal of the present study was to examine the contribution of thalamo-amygdala and thalamo-cortico-amygdala projections to fear conditioning. Lesions were used to destroy either the thalamo-cortico-amygdala projection, the thalamo-amygdala projection, or both projections, and the effects of such lesions on the acquisition of conditioned fear responses (changes in arterial pressure and freezing behavior) to a tone paired with footshock were measured. In each group of animals examined, a large lesion of the acoustic thalamus, including all nuclei of the medial geniculate body and adjacent portions of the posterior thalamus, was made on one side of the brain to block auditory transmission to the forebrain at the level of the thalamus on that side. In this way, experimental lesions could be made on the contralateral side of the brain. Thus, animals with thalamo-amygdala pathway lesions received a large lesion of the acoustic thalamus on one side. Contralaterally, only the nuclei that project to the amygdala (the medial division of the medial geniculate body, the posterior intralaminar nucleus, and the suprageniculate nucleus) were selectively destroyed, leaving much of the thalamo-cortico-amygdala projection intact. For thalamo-cortico-amygdala pathway lesions, the acoustic thalamus was destroyed on one side and temporal and perirhinal cortices were ablated contralaterally. In these animals, thalamo-amygdala projections were intact on the side of the cortical lesion. Destruction of either pathway alone had no effect on auditory fear conditioning. However, combined lesions of the two sensory pathways disrupted conditioning.(ABSTRACT TRUNCATED AT 250 WORDS)

Amygdala↗
PubMed1997

Emotion, olfaction, and the human amygdala: amygdala activation during aversive olfactory stimulation.

Electrophysiologic and lesion studies of animals increasingly implicate the amygdala in aspects of emotional processing. Yet, the functions of the human amygdala remain poorly understood. To examine the contributions of the amygdala and other limbic and paralimbic regions to emotional processing, we exposed healthy subjects to aversive olfactory stimuli while measuring regional cerebral blood flow (rCBF) with positron emission tomography. Exposure to a highly aversive odorant produced strong rCBF increases in both amygdalae and in the left orbitofrontal cortex. Exposure to less aversive odorants produced rCBF increases in the orbitofrontal cortex but not in the amygdala. Change of rCBF within the left amygdala and the left OFC was highly intercorrelated, indicating a strong functional interaction between these brain regions. Furthermore, the activity within the left amygdala was associated significantly with subjective ratings of perceived aversiveness. These findings provide evidence that the human amygdala participates in the hedonic or emotional processing of olfactory stimuli.

Adult↗
PubMed2003

Effects of left amygdala lesions on respiration, skin conductance, heart rate, anxiety, and activity of the right amygdala during anticipation of negative stimulus.

The present study reports the effects of lesions in the left amygdala on anxiety, respiration, skin conductance, heart rate, and electrical potentials in the right amygdala in two patients. Trait and anticipatory-state anxiety were measured before and after left amygdala resection to control medically intractable epilepsy in the patients. Lesions in the left amygdala resulted in decreases of trait and state anxiety, respiratory rate, and activity in the right amygdala in both patients; one patient also showed notable decreases in skin conductance and heart rate. The study also reports that activities in the right amygdala before the lesion were not observed after the lesion. We suggest that the activity of the right amygdala is dominantly activated in anxiety and anxiety-related physiological responses but needs excitatory inputs from the left amygdala.

Adult↗
PubMed1994

Task-dependent effects of intra-amygdala morphine injections: attenuation by intra-amygdala glucose injections.

Intraseptal injections of morphine impair learning and memory in rats, and these impairments are reversed by intraseptal injections of glucose. With evidence that injections of morphine into the amygdala also impair memory for some tasks, the present experiment determined whether (1) intra-amygdala morphine injections impair performance in inhibitory avoidance and spontaneous alternation tasks, and (2) intra-amygdala glucose injections attenuate the effects of intra-amygdala morphine injections. Rats receiving bilateral injections of morphine (4.0 nmol) into the amygdala, 30 min prior to training in inhibitory avoidance, had retention latencies significantly lower than those of unoperated and CSF controls when tested 24 hr later. Bilateral morphine injections (4.0 or 8.0 nmol) 30 min prior to testing in a spontaneous alternation task did not alter performance. The morphine-induced impairment observed in inhibitory avoidance was not due to diffusion up the cannulas, altered sensitivity to shock, or seizure activity. A glucose dose of 16.67 nmol, but not 8.33 nmol, injected into the amygdala attenuated the morphine-induced deficit in inhibitory avoidance. Rats receiving CSF into the amygdala exhibited decreased retention latencies in inhibitory avoidance compared to those of unoperated controls. This decrease was not attenuated by glucose at doses of 8.33 and 16.67 nmol. Therefore, these findings suggest that the amygdala is another brain region in which glucose affects brain functions, possibly by interacting with the opioid system and/or other neurotransmitter systems.

Amygdala↗
PubMed1993

Amygdala-hypothalamic control of feeding behavior in monkey: single cell responses before and after reversible blockade of temporal cortex or amygdala projections.

Single unit activity in the monkey amygdala and the lateral hypothalamic area was recorded during an operant feeding task. The task required discrimination of food, non-food, rewarding, aversive, novel, and familiar objects. Correct discriminations were rewarded with food or juice. Some amygdala neurons responded to the sight of objects in a graded manner that depended on the degree of affective significance of the object. Some neurons in the lateral hypothalamus responded to reward predicting objects, such as the sight of some non-food item that had been associated with juice reward. Neuronal responses to the sight of objects were influenced by extinction or reversal tests. Responses in the amygdala depended on extent of the affect or value of the reward and responses in the lateral hypothalamus depended on positive reinforcement. Information processing in the inferotemporal cortex--amygdala--lateral hypothalamus axis was identified by reversible changes induced in the temporal cortex or amygdala by cooling. The results suggest that the amygdala contributes to stimulus--affect associations and that the lateral hypothalamus is related directly to the initiation or termination of feeding through learning of stimulus-reinforcement association and/or maintenance of homeostasis. In addition the results suggest that the amygdala does more sensory processing than the lateral hypothalamus.

Amygdala↗
PubMed1996

The alpha 2-adrenoreceptor agonist clonidine suppresses seizures, whereas the alpha 2-adrenoreceptor antagonist idazoxan promotes seizures in amygdala-kindled kittens: a comparison of amygdala and pontine microinfusion effects.

PURPOSE: We sought to determine whether local, in vivo microinfusion of an alpha 2-adrenoreceptor agonist and antagonist into either the amygdala or the pons (locus ceruleus, LC) would have contrasting effects on evoked amygdala-kindled seizure susceptibility. METHODS: The study population consisted of 6 amygdala-kindled kittens, each undergoing the same protocol, in which the amygdala microinfusion paradigm preceded the pontine microinfusion series. Microinfusions (1 microliter) of the alpha 2-agonist clonidine (CLON) and the alpha 2-antagonist idazoxan (IDA) were made over 1 min through cannulas adjacent to stimulating electrodes in the kindled amygdala or through cannulas adjacent to recording electrodes in the ipsilateral LC. Order of administered drugs (CLON vs. IDA) and dosages (n = 3 each) was partly counterbalanced. Focal and convulsive seizure thresholds were evaluated 10-12 min postinfusion and compared to thresholds obtained during two interspersed control conditions (vehicle control = 1 microliter microinfusion of sterile saline; sham control = needle insertion only). RESULTS: CLON significantly increased focal and generalized seizure thresholds, whereas IDA significantly reduced seizure thresholds when compared to controls. Magnitude of effects was dose dependent and more potent after pontine than amygdala microinfusion. CONCLUSIONS: Our results confirm and extent findings of previous researchers who used unlocalized in vivo manipulations to show that norepinephrine (NE) is a highly antiepileptic agent in the amygdala kindling preparation. With further investigation, the results may ultimately lead to development of microinfusion techniques as an alternative treatment option for limbic epilepsy.

Adrenergic alpha-Agonists↗
PubMed1990

Involvement of amygdala pathways in the influence of post-training intra-amygdala norepinephrine and peripheral epinephrine on memory storage.

These experiments examined the role of two major amygdala afferent-efferent pathways--the stria terminalis (ST) and the ventral amygdalofugal pathway (VAF)--in mediating the effects, on memory storage, of post-training intra-amygdala injections of norepinephrine (NE) and subcutaneous (s.c.) injections of epinephrine (E). Rats with either ST lesions or VAF transections and sham-operated rats were trained on a one-trial step-through inhibitory avoidance task and immediately after training received intra-amygdala injections of NE or a buffer solution. Other groups of VAF-transected animals received post-training s.c. injections of E or saline. ST lesions blocked the memory-enhancing effect of intra-amygdala injections of a low dose of NE (0.2 microgram) as well as the amnestic effect of a high dose of NE (5.0 microgram). In contrast, VAF transections did not block the memory-enhancing effect of NE (0.2 microgram). However, VAF transections attenuated the memory-enhancing effect of s.c. injections of E: the effective dose of E was shifted from 0.1 to 0.5 mg/kg. These findings, considered together with previous evidence that ST lesions block the memory-enhancing effect of peripheral E injections, suggest that the VAF is involved in mediating the central influence of peripheral E on amygdala functioning, while the ST is involved in mediating amygdala influences on memory storage elsewhere in the brain.

Amygdala↗
PubMed1999

FAST and SLOW amygdala kindling rat strains: comparison of amygdala, hippocampal, piriform and perirhinal cortex kindling.

In our companion paper, we selectively bred offspring of a Long Evans Hooded and Wistar rat cross for either fast or slow rates of amygdala kindling (Racine et al., 1999. Development of kindling-prone and kindling resistant rats: Selective breeding and electrophysiological studies, Epilepsy Res. 35, 183-195). Within 10 generations, there was no overlap in the distribution of kindling rates between these newly developed FAST and SLOW kindling strains. In the present report, we compared the local excitability, kindling rates, and convulsion profiles of kindling sites in either the amygdala, dorsal hippocampus, piriform cortex or perirhinal cortex in the two strains. Local excitability, measured as the local afterdischarge (AD) threshold and its duration, showed varied effects between structures and strains. Before kindling, the AD threshold was lower in the FAST than the SLOW rats in the hippocampus, piriform and perirhinal cortices, but not the amygdala (the selection structure). Also, the duration of the AD threshold duration was significantly longer in the FAST than in the SLOW rats in all structures, except the CA1 hippocampus. Most of these differences were maintained after kindling. Kindling itself was significantly faster in the FAST compared with the SLOW rats in all structures; however, the different structural kindling rates showed proportional differences between strains that were about five times different in the amygdala compared with only about two times different in the hippocampus. This suggested a selection bias for the amygdala and its networks. As in other rat strains, the fastest kindling rates were seen in the perirhinal cortex followed by the piriform cortex, amygdala and hippocampus in both FAST and SLOW rats. Other important differences between strains and structures occurred in the stage-5 convulsion profiles, including latency to forelimb clonus, clonus duration and duration of associated local afterdischarges. The differences in kindling profiles between strains and structures were discussed with respect to possible underlying mechanisms, significance for epileptogenesis, and impact on other normal behaviours.

Amygdala↗
PubMed2003

Development and subunit composition of synaptic NMDA receptors in the amygdala: NR2B synapses in the adult central amygdala.

NMDA receptors are well known to play an important role in synaptic development and plasticity. Functional NMDA receptors are heteromultimers thought to contain two NR1 subunits and two or three NR2 subunits. In central neurons, NMDA receptors at immature glutamatergic synapses contain NR2B subunits and are largely replaced by NR2A subunits with development. At mature synapses, NMDA receptors are thought to be multimers that contain either NR1/NR2A or NR1/NR2A/NR2B subunits, whereas receptors that contain only NR1/NR2B subunits are extrasynaptic. Here, we have studied the properties of NMDA receptors at glutamatergic synapses in the lateral and central amygdala. We find that NMDA receptor-mediated synaptic currents in the central amygdala in both immature and mature synapses have slow kinetics and are substantially blocked by the NR2B-selective antagonists (1S, 2S)-1-(4-hydroxyphenyl)-2-(4-hydroxy-4-phenylpiperidino)-1-propano and ifenprodil, indicating that there is no developmental change in subunit composition. In contrast, at synapses on pyramidal neurons in the lateral amygdala, whereas NMDA EPSCs at immature synapses are slow and blocked by NR2B-selective antagonists, at mature synapses their kinetics are faster and markedly less sensitive to NR2B-selective antagonists, consistent with a change from NR2B to NR2A subunits. Using real-time PCR and Western blotting, we show that in adults the ratio of levels of NR2B to NR2A subunits is greater in the central amygdala than in the lateral amygdala. These results show that the subunit composition synaptic NMDA receptors in the lateral and central amygdala undergo distinct developmental changes.

Amygdala↗
PubMed1992

Amygdala kindling does not alter the N-methyl-D-aspartate receptor-channel complex which modulates dopamine release in the rat striatum and amygdala.

Kindling is suggested to be critically associated with enhancement of N-methyl-D-aspartate (NMDA) type excitatory amino acid synaptic transmission. The present study examined effects of kindling on NMDA-induced dopamine (DA) efflux from slices of the rat striatum and amygdala. When assayed 5-7 days after the last evoked seizure, no difference was observed between kindled and non-kindled striatum in the ability of NMDA to induce DA release, or in the effect of MK-801 or 7-chlorokynurenic acid to inhibit the amino acid-induced transmitter release. The present study revealed that NMDA receptors are also involved in the modulation of DA release in the amygdala. However, no difference was observed between kindled and non-kindled amygdala in the ability of NMDA to induce DA release. These results suggest that amygdala kindling does not alter activity of the NMDA receptor-channel complex modulating DA release in the striatum and amygdala.

Amygdala↗
PubMed2001

Monoamines and seizures: microdialysis findings in locus ceruleus and amygdala before and during amygdala kindling.

We used microdialysis to determine extracellular concentrations of norepinephrine (NE), dopamine (DA) and serotonin (5-HT) before and during a 1-day amygdala kindling paradigm. Subjects were young cats (<1 year old; n=8; 6 female, 2 male). Consecutive 5-min samples (2 microl/min infusion rate) were obtained from left amygdala and ipsilateral locus ceruleus complex (LC) under 3 experimental conditions lasting 1-h each (n=12 samples per cat per condition): (1) just before amygdala stimulation (baseline), (2) during focal afterdischarge (AD) and (3) during generalized AD. ADs were elicited by electrical stimulation applied to establish thresholds immediately before dialysate collection as well as during each sample collected in focal vs. generalized AD conditions. Sample concentrations were time-adjusted to correspond with sleep vs. waking state and/or focal vs. generalized ADs. Seizure activity was indexed by AD threshold (mA) and duration (s) as well as number and duration of specific clinically evident (behavioral) seizure manifestations. Main results were: (1) Lower baseline concentrations (fmoles per sample) of NE, DA and 5-HT correlated with subsequent increases in duration of focal and generalized AD as well as number of behavioral seizure correlates. (2) When compared to baseline levels, NE, DA and 5-HT concentrations significantly increased only in amygdala during focal AD and in both amygdala and LC during generalized AD. (3) NE and 5-HT concentrations were higher than DA at both collection sites and were selectively associated with increased wakefulness throughout the study.

Amygdala↗
PubMed1996

Evidence for membrane remodeling in ipsilateral thalamus and amygdala following left amygdala-kindled seizures in awake rats.

We examined regional cerebral metabolic rates for glucose (rCMRglc) and brain incorporation coefficients (k*) of each of three intravenously infused fatty acid radiotracers, [9,10-(3H)]palmitate ([3H]PAM), [1-(14C)]arachidonate ([14C]AA) and [1-(14C)]docosahe-xaenoate ([14C]DHA), in awake rats fully kindled by once-daily electrical stimulation of the left amygdala. Compared with sham-stimulated animals, rCMRglc was increased bilaterally during a seizure, particularly in midbrain-brain stem regions, thalamus and basolateral nucleus of the amygdala. At 24 h and 2 weeks after a seizure, there was no significant change in k* for either [14C]AA or [14C]DHA in any brain region, whereas k* for [3H]PAM at 24 h was increased significantly (by 32-53%) ipsilateral to stimulation in regions of the amygdala and thalamus. Contralateral regions showed no significant change. Two weeks after a seizure, k* for [3H]PAM was increased in the ipsilateral lateral dorsal nucleus of the thalamus. These results argue for membrane remodeling involving phosphatidylcholine in the ipsilateral amygdala and thalamus at the completed phase of amygdala kindling. Remodeling may continue for up to 2 weeks after a seizure during the completed phase.

Amygdala↗
PubMed1981

Connections of the corticomedial amygdala in the golden hamster. I. Efferents of the "vomeronasal amygdala".

The medial (M) an posteromedial cortical (C3) amygdaloid nuclei and the nucleus of the accessory olfactory tract (NAOT) are designated the "vomeronasal amygdala" because they are the only components of the amygdala to receive a direct projection from the accessory olfactory bulb (AOB). The efferents of M and C3 were traced after injections of 3H-proline into the amygdala in male golden hamsters. Frozen sections of the brains were processed for autoradiography. The efferents of the "vomeronasal amygdala" are largely to areas which are primary and secondary terminal areas along the vomeronasal pathway, although the efferents from C3 and M terminate in different layers in these areas than do the projections from the vomeronasal nerve or the AOB. Specifically, C3 projects ipsilaterally to the internal granule cell layer of the AOB, the cellular layer of NAOT, and layer Ib of M. Additional fibers from C3 terminate in a retrocommissural component of the bed nucleus of the strain terminalis (BNST) bilaterally, and in the cellular layers of the contralateral C3. The medial nucleus projects to the cellular layer of the ipsilateral NAOT, layer Ib of C3, and bilaterally to the medial component of BNST. Projections from M to non-vomeronasal areas terminate in the medial preoptic area-anterior hypothalamic junction, ventromedial nucleus of the hypothalamus, ventral premammillary nucleus and possibly in the ventral subiculum. These results demonstrate reciprocal connections between primary and secondary vomeronasal areas between the secondary areas themselves. They suggest that M, but not C3, projects to areas outside this vomeronasal network. The medial amygdaloid nucleus is therefore an important link between the vomeronasal organ and areas of the brain not receiving direct vomeronasal input.

Amygdala↗
PubMed1981

Connections of the corticomedial amygdala in the golden hamster. II. Efferents of the "olfactory amygdala".

The anterior cortical (C1) and posterolateral cortical (C2) nuclei of the amygdala are designated the "olfactory amygdala" because they each receive direct projections from the main olfactory bulb. The efferents of these nuclei were traced after stereotaxic placement of 1-5 muCi tritiated proline in the corticomedial amygdala of the male golden hamsters. Following survival times of 12, 24, or 48 hours, 20 micron frozen sections of the brains were processed for light microscopic autoradiography. Efferents from C2 terminate in layers II and III of the olfactory tubercle and in layer Ib of pars ventralis and pars medialis of the anterior olfactory nucleus. Fibers from this nucleus also project to layers I and II of the infralimbic cortex and to the molecular layer of the agranular insular cortex. More posteriorly, fibers from C2 terminate in layer I of the dorsolateral entorhinal cortex, and in the endopiriform nucleus. From C1, efferent fibers travel in the stria terminalis and terminate in the precommissural bed nucleus of the stria terminalis and in the mediobasal hypothalamus. Efferents from C1 also innervate the molecular layer of C2, the amygdalo-hippocampal area, and the adjacent piriform cortex. Neurons in both C1 and C2 project to the molecular layer of the medial amygdaloid nucleus and the posteromedial cortical nucleus of the amygdala, the plexiform layer of the ventral subiculum, and the molecular layer of the lateral entorhinal cortex.

Amygdala↗
PubMed2005

Antinociception following application of DAMGO to the basolateral amygdala results from a direct interaction of DAMGO with Mu opioid receptors in the amygdala.

Previous studies from our laboratory have shown that application of the mu opioid agonist DAMGO into the basolateral region of the amygdala (BLA) suppresses the radiant heat tail flick (TF) reflex in anesthetized rats. This antinociceptive effect can be blocked by lesions of brainstem regions such as the periaqueductal gray (PAG) or the rostral ventromedial medulla (RVM) or by functional inactivation of neurons in these regions, suggesting the activation of brainstem-descending antinociceptive systems from the amygdala. However, little is known about the direct interaction of DAMGO with mu receptors in the amygdala. In the present series of experiments, the BLA was pretreated with opioid receptor antagonists and a G protein inhibitor prior to TF testing with application of DAMGO into the same site. Rats pretreated with the non-selective opioid antagonist naltrexone (1.25-3.75 microg/0.25 microl per side) or the G protein inhibitor pertussis toxin (0.25 microg) failed to show inhibition of TF reflexes following infusion of DAMGO (0.168-0.50 microg), indicating that DAMGO works through G-protein-coupled opioid receptors in the BLA. Furthermore, pretreatment with the mu antagonist beta-FNA (1.00-2.00 microg) attenuated antinociception induced by DAMGO injection, suggesting DAMGO's action on mu receptors in the BLA. Accordingly, we confirm a direct interaction of DAMGO with G-protein-coupled mu receptors in the BLA contributing to induction of opioid antinociception in the amygdala.

Amygdala↗