Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “AMYGDALOID BODY”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 523 records · Page 29Linked to original sources
PubMed1980

Immunoreactive adrenocorticotropin in rat brain: a neuroanatomical study using antiserum generated against synthetic ACTH.

In this study an antiserum generated against synthetic ACTH1--39 is used to provide a neuroanatomical map of ACTH-immunoreactivity in rat brain. Groups of ACTH-immunoreactive cell bodies were located in the basal hypothalamus, extending from the retrochiasmatic region to the mammillary nuclei. The fiber distribution indicates a broad innervation of structures in the hypothalamus, which include the medial preoptic region; bed nucleus of the anterior commissure and stria terminalis; perifornical region; periventricular stratum; and paraventricular, dorsomedial, arcuate, and mammillary nuclei. Fibers from the hypothalamus reach the amygdaloid nuclei directly in two separate bundles. A large dorsal ACTH-immunoreactive bundle emerges from the anterior hypothalamic region, distributes to the periventricular thalamic nuclei, and continues more posteriorly to the midbrain periaquaductal gray. It is speculated that the cell bodies in the ventral tuberal region of the hypothalamus are responsible for the vast innervation of fibers to the forebrain, diencephalon, and brainstem.

Adrenocorticotropic Hormone↗
PubMed1999

Estrogen receptor immunoreactivity within subregions of the rat forebrain: neuronal distribution and association with perikarya containing choline acetyltransferase.

Administration of the neuroactive steroid hormone estrogen has been shown to effect cholinergic basal forebrain neuronal function. Antibodies directed against the estrogen receptor alpha (ERalpha) revealed dark (type 1) and light (type 2) nuclear positive neurons within the islands of Calleja, endopiriform nucleus, lateral septum, subfields of the cholinergic basal forebrain, bed nucleus of the stria terminalis, striohypothalamic region, medial preoptic region, periventricular, ventromedial, arcuate and tuberal mammillary nuclei of the hypothalamus, reuniens and anterior medial thalamic nuclei, amygdaloid complex, piriform cortex and subfornical organ. In contrast, only a few scattered ERalpha labeled neurons were found in cortex and hippocampus. ERalpha stained cell bodies were not seen in the striatum. Counts of ERalpha labeled neurons in intact female rats revealed significantly more type 2 neurons within the basal forebrain subfields. Quantitation of ERalpha immunoreactive neurons revealed a significant decrease in the relative number of type 1 neurons within the medial septum (MS), horizontal limb of the diagonal band (HDB) and substantia innominata/nucleus basalis (SI/NB) following ovariectomy. Quantitation following choline acetyltransferease (ChAT) immunohistochemistry revealed a significant decrease in the number of ChAT positive neurons within the MS, HDB and SI/NB, but not VDB following ovariectomy. Following ovx, the percentage of double labeled cholinergic basal forebrain neurons also declined significantly within the MS, VDB, HDB and SI/NB. These observations suggest that estrogen effects a subpopulation of cholinergic basal forebrain neurons and may provide insight into the biologic actions of this steroid in Alzheimer's disease.

Animals↗
PubMed2003

Regional distribution of alpha-synuclein pathology in unimpaired aging and Alzheimer disease.

The amygdaloid complex (AC) was found highly vulnerable to alpha-synuclein (alphaS) pathology in both familial and sporadic Alzheimer disease (AD), and recently, incidental Lewy bodies (LBs) were identified primarily in the lower brainstem. This challenges the traditional view that the substantia nigra (SN) is the region that is predominately affected in the spectrum of LB disorders. We examined the immunoreactivity of alphaS in the SN, the nucleus basalis of Meynert (nbM), and the AC in 904 subjects with or without concomitant AD pathology. AlphaS-positive structures were seen in at least one of the studied brain areas in 121 subjects (13%). The affected regions in the alphaS-positive subjects included the SN (89%), the nbM (73%), and the AC (67%). This study also included 82 sporadic AD patients diagnosed using CERAD criteria. AlphaS-positive structures were seen in 32% of the AD patients, with the SN and AC being equally affected. In a few subjects the AC was the only affected area. However, this was not inevitably associated with AD pathology, but was related to cognitive decline. Incidental LBs in the SN were described in the occasional subjects, with no alphaS pathology in the lower brainstem.

Adult↗
PubMed1991

Computer-assisted mapping of immunoreactive mammalian gonadotropin-releasing hormone in adult human basal forebrain and amygdala.

Immunocytochemistry performed on 80-microns unembedded tissue sections was used to study the localization of GnRH-containing neurons and fibers in the basal forebrain and amygdala of six adult (four male, two female) human brains. Sections from one of the female brains were subjected to computer-assisted microscopic mapping to generate a three-dimensional analysis of immunoreactive structures. In all six brains examined, cell bodies were concentrated in the preoptic area and basal hypothalamus, but were also evident in the septal region, anterior olfactory area, and cortical and medial amygdaloid nuclei. GnRH-containing fibers were observed within the hypothalamus (predominantly infundibular region and preoptic area), septum, stria terminalis, ventral pallidum, dorsomedial thalamus, olfactory stria, and anterior olfactory area. Many fibers could also be seen coursing along the base of the brain between the hypothalamus and cortical and medial amygdaloid nuclei. The localization of GnRH-containing cells and fibers in several of these areas represents new observations in the human brain and suggests a role for the amygdaloid complex in the regulation of gonadotropin secretion. The comprehensive view provided by these data may be useful in the clinical application of novel transplantation strategies.

Adult↗
PubMed2003

Distribution of NTS3 receptor/sortilin mRNA and protein in the rat central nervous system.

The neurotensin (NT) receptor, NTS3, originally identified as the intracellular sorting protein sortilin, is a member of a recently discovered family of receptors characterized by a single transmembrane domain. The present study provides the first comprehensive description of the distribution of NTS3/sortilin mRNA and protein in adult rat brain using in situ hybridization and immunocytochemistry. Both NTS3/sortilin mRNA and immunoreactivity displayed a widespread distribution throughout the brain. High levels of NTS3/sortilin expression and immunoreactivity were found in neuronal cell bodies and dendrites of allocortical areas such as the piriform cortex and hippocampus. Regions expressing both high levels of NTS3/sortilin mRNA and protein also included several neocortical areas, the islands of Calleja, medial and lateral septal nuclei, amygdaloid nuclei, thalamic nuclei, the supraoptic nucleus, the substantia nigra, and the Purkinje cell layer of the cerebellar cortex. In the brainstem, all cranial nerve motor nuclei were strongly labeled. NTS3/sortilin mRNA and immunoreactivity were also detected over oligodendrocytes in major fiber tracts. Subcellularly, NTS3/sortilin was predominantly concentrated over intracytoplasmic membrane-bound organelles. Many of the areas exhibiting high levels of NTS3/sortilin (e.g., olfactory cortex, medial septum, and periaqueductal gray) have been documented to contain high concentrations of NT nerve cell bodies and axons, supporting the concept that NTS3/sortilin may play a role in NT sorting and/or signaling. Other areas (e.g., hippocampal CA fields, cerebellar cortex, and cranial nerve motor nuclei), however, are NT-negative, suggesting that NTS3/sortilin also exerts functions unrelated to NT signaling.

Adaptor Proteins, Vesicular Transport↗
PubMed2004

Prolongation of T(2) relaxation times of hippocampus and amygdala in Alzheimer's disease.

There exists controversy on the MR T(2) relaxometry of hippocampus in Alzheimer's disease (AD). The aim of our study was to examine whether there was a prolonged T(2) relaxation time (T(2)) in hippocampus and amygdala in AD, and whether in AD, the relaxometry data correlated to cognitive performance. In a 1.5 T MR scanner, T(2) of hippocampus and amygdala was measured from 51 patients with AD, 23 subjects with vascular dementia (VaD) and 31 healthy elderly controls. The cognitive performance was assessed with the Alzheimer's Disease Assessment Scale - Cognitive Subscale (ADAS-Cog). The AD patients had longer T(2) in hippocampus and amygdala than VaD subjects and healthy elderly controls. In AD, the right hippocampal T(2) was correlated with ADAS-Cog scores, whereas amygdaloid T(2) was not.

Aged↗
PubMed1995

Neuropeptide Y and somatostatin-like immunoreactivity in neurons of the monkey amygdala.

Neurons in the monkey amygdala exhibiting neuropeptide Y-like immunoreactivity and somatostatin-like immunoreactivity were identified using an avidin-biotin immunohistochemical technique. Differential co-existence of the two peptides was demonstrated using two-color immunoperoxidase and adjacent section methods. Numerous neuropeptide Y-positive neurons were observed in the basolateral and superficial amygdaloid nuclei. A moderate number of neuropeptide Y-positive neurons was seen in the medial subdivision of the central nucleus, but only a few neurons were observed in the lateral subdivision. Numerous somatostatin-positive neurons were stained in all major amygdaloid nuclei and always outnumbered neuropeptide Y-positive cells. All amygdaloid nuclei contained numerous peptide-positive fibers whose density varied depending on the nucleus. Approximately 90% of neuropeptide Y-positive neurons also exhibited somatostatin-like immunoreactivity. The percentage of somatostatin-positive neurons that exhibited neuropeptide-Y immunoreactivity varied in different nuclei. In the superficial amygdaloid nuclei, medial subdivision of the central nucleus and most portions of the basolateral nuclei the predominant cell type stained with both the neuropeptide Y and somatostatin antibodies was a spine-sparse non-pyramidal neuron. In the dorsal portion of the lateral nucleus, however, most peptide-positive neurons had spiny dendrites. Only the cell bodies and proximal dendrites of somatostatin-positive neurons in the lateral subdivision of the central nucleus were immunostained. This study demonstrates that specific cell populations in the primate amygdala contain neuropeptide Y, somatostatin or both peptides. Most peptide-positive neurons in the basolateral and superficial amygdaloid nuclei appear to be local circuit neurons that contribute to the dense plexus of peptide-positive axons in these regions. The finding of neurons with spiny dendrites in the dorsal part of the lateral nucleus suggests that these cells may be functionally different from peptide-positive neurons in other portions of the basolateral amygdala. The lateral subdivision of the central nucleus is distinguished from other amygdaloid nuclei by containing a large population of somatostatin-positive neurons that do not exhibit neuropeptide Y immunoreactivity.

Amygdala↗
PubMed1995

Involvement of subcortical and cortical afferents to the lateral nucleus of the amygdala in fear conditioning measured with fear-potentiated startle in rats trained concurrently with auditory and visual conditioned stimuli.

The goal of this work was to test the involvement, in fear conditioning, of afferents to the lateral nucleus of the amygdala originating from the auditory thalamus, auditory cortex, and perirhinal area. The acoustic startle reflex was used as the behavioral index of conditioning because it is reliably enhanced in the presence of a conditioned stimulus (CS) previously paired with a footshock. Auditory and visual CSs were used to assess the modality specificity of lesions to the above brain areas. Pre- or posttraining lesions of the entire auditory thalamus including the ventral, dorsal, and medial divisions of the medial geniculate body, the posterior intralaminar nucleus, and the suprageniculate nucleus, completely blocked fear-potentiated startle to the auditory CS, but had no effect on fear-potentiated startle to the visual CS. Posttraining lesions mostly restricted to the ventral and dorsal divisions of the medial geniculate body specifically disrupted fear-potentiated startle to the auditory CS. However, retraining in rats sustaining ventral and dorsal medial geniculate body lesions led to reliable fear-potentiated startle to the auditory CS. Posttraining lesions mostly restricted to the medial division of the medial geniculate body, posterior intralaminar, and suprageniculate nuclei did not disrupt fear-potentiated startle. These results indicate that the auditory thalamus is specifically involved, through either its direct or indirect amygdaloid afferents, in fear conditioning to auditory CSs. Pre- or posttraining lesions mostly restricted to the primary auditory cortex did not reliably attenuate fear-potentiated startle to the auditory or visual CSs. Extensive posttraining lesions of the perirhinal area (including secondary auditory cortices), but not its rostral aspect alone, blocked fear-potentiated startle to both CSs. However, reliable potentiated startle was observed to both CSs following similarly extensive pretraining lesions of the perirhinal area. Because post- but not pretraining lesions of the perirhinal area blocked fear-potentiated startle nonspecifically, at least with regard to auditory and visual CSs, the results are consistent with the involvement of the perirhinal area in general memory functions such as information storage or retrieval. Alternatively, the secondary auditory and/or perirhinal cortices might function as multimodal sensory relays to the amygdala.

Acoustic Stimulation↗
PubMed1981

Brain lesions in infant female rhesus monkeys: effects on menarche and first ovulation and on diurnal rhythms of prolactin and cortisol.

Sexual maturation in female rhesus macaques was studied after surgical isolation of the medial basal hypothalamus [complete hypothalamic disconnection (CHD); n = 4] or after creation of amygdaloid lesions (AMYG; n = 6). In four animals, CHD at 8 months did not affect the age when menarche occurred (30 months) but did result in a significant (P less than 0.01) advancement in age at first ovulation (35.8 +/- 1.1 vs. 43.7 +/- 1.1 months for the five controls). Body weights in CHD and AMYG animals were not different from weights of controls at either menarche or first ovulation, but CHD animals gained weight faster than controls. Although there was no overall difference in age at menarche or first ovulation between AMYG animals and controls, the three AMYG animals that sustained damage to the corticomedial amygdaloid area ovulated later than three other AMYG animals without damage to this area. Daily serum levels of LH, FSH, and 17 beta-estradiol were measured in the second ovulatory cycle of each animal and found to be similar among the three groups. Serum progesterone levels revealed that three of the five controls and one of six AMYG animals had short luteal phases typical of pubertal monkeys, whereas all four CHD animals showed luteal phases typical of sexually mature adult animals. Serum cortisol and PRL showed significant diurnal changes in all three groups. These data indicate that in infant rhesus females, intact neural connections to the medial basal hypothalamus are not obligatory for sexual maturation or for the propagation of entrained diurnal rhythms in cortisol and PRL. That isolation of the medial basal hypothalamus resulted in an increase in the rate of weight gain and favored early sexual maturation may indicate that the main effect of the higher brain centers is inhibitory on hypothalamic mechanisms which control these processes.

Amygdala↗
PubMed1980

Vasoactive intestinal polypeptide (VIP) in mouse and rat brain: an immunocytochemical study.

Immunoperoxidase technique and light microscopy were used to investigate the distribution of vasoactive intestinal polypeptide (VIP) in mouse and rat brain. Both 50 micrometers unmounted cryostat and 6 micrometers deparaffinized sections were studied in coronal or sagittal plane. At least 4 different major VIP systems were found: (1) an intracerebral cortical system; (2) one innervating the central amygdala and nucleus of the stria terminalis; (3) a pathway originating in the suprachiasmatic nucleus of the hypo thalamus; and (4) another originating in the central grey of the midbrain. Specific cell body staining was seen in the limbic and neocortex, in the basal-caudal portion of the suprachiasmatic nucleus of the hypothalamus, and in the central grey of the midbrain. Heavy terminal field patterns were noted in the suprachiasmatic nucleus, central amygdaloid nucleus, bed nucleus of the stria terminalis and nucleus accumbens. Fiber density was moderate in the tuberculum olfactoriu, anterior hypothalamus including the medial preoptic area, mediobasal hypothalamus (especially dorsomedial region), periventricular thalamus, lateral lemniscal system, parabrachial nucleus, nucleus solitarius, and area postrema. Fibers could be traced dorsally from the suprachiasmatic nucleus to the dorsomedial and paraventricular nuclei of the hypothalamus and the periventricular nucleus of the thalamus. Scattered cell bodies and fibers were found in a number of other forebrain and brain stem areas with only a rare fiber seen in median eminence.

Amygdala↗
PubMed1988

Penile hyperexcitability with recurrent ejaculations as the presenting manifestation of a case of rabies.

A patient with rabies presented with penile hypersensitivity and recurrent ejaculation. This preceded the more classical manifestations such as hydrophobia and aerophobia by approximately 8 hours. A review of the literature reveals that a variety of urogenital symptoms may rarely occur in rabies. Ours is however the first report documenting the occurrence of these symptoms at the onset of the disease in an autopsy proven case of rabies. Damage to the amygdaloid nucleus has been postulated to be the basis of these urogenital symptoms. This correlates well with our autopsy findings of extensive neuronal damage and Negri bodies in the temporal poles.

Ejaculation↗
PubMed1993

Distribution of GABA immunoreactivity in the amygdaloid complex of the cat.

This study describes the distribution of GABA immunoreactivity in the amygdaloid complex of cats. At the light microscopic level, immunopositive structures consisted of morphologically diverse somata and numerous small punctate elements. The latter accounted for most of the staining at low magnification and, at the electron microscopic level, were found to be axon terminals establishing symmetric synaptic contacts with a variety of postsynaptic profiles. Deep and superficial amygdaloid nuclei could be assigned to one of four groups according to (i) the intensity of immunolabeling they displayed, (ii) their density in reactive somata, and (iii) the size of the immunopositive somata they contained. Intercalated cell masses displayed the highest density of strongly immunoreactive cell bodies and presumed GABAergic terminals. However, electron microscope observations showed that intercalated somata were almost devoid of synaptic contacts. In contrast, central and medial nuclei were characterized by a low density of intensely immunoreactive somata and an elevated concentration for GABAergic terminals which contacted somatic and dendritic profiles. In addition, central and medial nuclei contained numerous neurons displaying low to moderate immunoreactivity. Superficial amygdaloid nuclei and nuclei of the basolateral complex displayed an intermediate density of immunoreactive somata and a low to moderate concentration of presumed terminals. Analysis of the distribution of soma areas within these nuclei revealed that the basolateral complex contains a distinct subpopulation of larger immunoreactive neurons. In light of recent electrophysiological findings, these results suggest that the intra-amygdaloid GABAergic system plays a major role in controlling the synaptic responsiveness and spontaneous activity of amygdaloid neurons.

Amygdala↗
PubMed1988

Immunocytochemical localization of glutamate decarboxylase in the rat basolateral amygdaloid nucleus, with special reference to GABAergic innervation of amygdalostriatal projection neurons.

Glutamate decarboxylase (GAD) immunohistochemistry was employed at the light and electron microscopic levels to localize GABAergic structures in the basolateral amygdaloid nucleus (BL). The GAD-immunoreactive (GAD-IR) staining pattern consisted of punctate structures and a morphologically diverse group of GAD-IR neurons. At the electron microscopic level many of these punctate structures were found to make symmetrical synaptic contacts with cell bodies as well as distal parts of unlabeled, presumably projection and nonprojection, neurons. In addition, GAD-immunoreactive neurons were identified in the BL, and they had the ultrastructural characteristics of local circuit or intrinsic neurons and were not retrogradely labeled with HRP following ventral striatal injections. Some of these GAD-immunoreactive neurons were contacted by GABAergic boutons, forming symmetrical synaptic contacts. GABAergic innervation of amygdaloid projection neurons in the BL was identified by combining GAD immunohistochemistry with Golgi impregnation and retrograde tracing of horseradish peroxidase (HRP) following injections of the tracer in the olfactory-tubercle-related parts of the ventral striatum. Amygdalostriatal projection neurons in the BL were observed to be in continuity with neurons in the piriform cortex which project to the ventral striatum. The results provide direct evidence for the presence of GAD-IR boutons in the BL making synaptic contacts with identified amygdalostriatal projection neurons. The present study provides direct anatomical evidence for the physiological observation that GABA exhibits a powerful regulation of the amygdaloid projection neurons in the BL and lends further support to the concept of a corticallike functional organization of the basolateral amygdala.

Amygdala↗
PubMed1982

Direct projections from the extrathalamic forebrain structures to the neocortex in the macaque monkey.

Extrathalamic direct projections from the subcortical forebrain structures to the neocortex were examined in the macaque monkey by the horseradish peroxidase method. The enzyme, when injected into discrete regions in the neocortex, labeled cell bodies of extrathalamic forebrain neurons in the basal nucleus of Meynert, nucleus of the diagonal band, medial septal nucleus, hypothalamus, claustrum and dorsolateral part of the basal amygdaloid nucleus. Neurons in the basal nucleus of Meynert, lateral hypothalamus and claustrum appeared to send their axons widely, but not diffusely, to the neocortex.

Animals↗
PubMed1994

Differential expression of the 61 kDa and 63 kDa calmodulin-dependent phosphodiesterases in the mouse brain.

Based on their relative abundance and regulation by Ca2+ and by phosphorylation in vitro, it is thought that the Ca2+/calmodulin-dependent phosphodiesterases (CaM-PDEs) are important modulators of cyclic nucleotide function in the brain. Two of the most abundant CaM-PDEs in the brain are the 61 kDa and 63 kDa isozymes. In this study, the regional and cellular expression of mRNA encoding these two different isoforms in mouse brain has been determined by in situ hybridization. The 63 kDa CaM-PDE mRNA has a wide-spread but uneven distribution. Very strong hybridization signals are present in the caudate-putamen, nucleus accumbens, olfactory tubercle, and dentate gyrus of the hippocampus. Somewhat lesser amounts of 63 kDa CaM-PDE mRNA are present in the olfactory bulb and piriform cortex. Weaker but still easily discernible hybridization signals are seen in several layers of the cerebral cortex, CA1 and CA3 regions of the hippocampus, amygdaloid nuclear complex, thalamus, hypothalamus, midbrain, brainstem, cerebellum, and spinal cord. A weak hybridization signal was detected in the globus pallidus of the basal ganglia. In general, the distribution of the 63 kDa CaM-PDE is very similar to that of dopamine receptors, suggesting that it may modulate dopamine function. In contrast, the 61 kDa CaM-PDE mRNA has a more limited and much different distribution, with the highest level of expression in the cerebral cortex and in the pyramidal cells of the hippocampus. A moderate hybridization signal was detected in the medial habenula and amygdaloid nuclear complex. In addition, small subsets of neurons in several other regions showed specific hybridization. Both PDE mRNAs appear to be localized exclusively in neuronal cell bodies. Their distinct distribution suggests important but different physiological roles for these two isozymes in the regional regulation of cyclic nucleotides in the CNS. Since these two isozymes are differentially phosphorylated by cAMP-dependent and Ca2+/CaM-dependent protein kinases, the differential expression also provides a potential mechanism by which these PDEs can differentially regulate cAMP and cGMP in different brain areas. The high expression levels in specific subsets of neurons also suggest that agents increasing Ca2+ in these neurons will increase the rate of cyclic nucleotide degradation.

Animals↗
PubMed1989

Organization and synaptic interconnections of GABAergic and cholinergic elements in the rat amygdaloid nuclei: single- and double-immunolabeling studies.

The aim of this study was to describe the localization of cholinergic and GABAergic neurons and terminals in the amygdaloid nuclei of the rat. Double immunolabeling was performed to study cholinergic-GABAergic synaptic interconnections. Cholinergic elements were labeled by using a monoclonal antibody to choline acetyltransferase (ChAT), the acetylcholine synthesizing enzyme. Antibodies against glutamate decarboxylase (GAD), the GABA- synthesizing enzyme, were employed to identify GABAergic perikarya and terminals. The tissue sites of the antibody bindings were detected by using either Sternberger's peroxidase-antiperoxidase (PAP) method or a biotinylated secondary antibody and avidinated ferritin. These two contrasting immunolabels allowed us to study GABAergic-cholinergic interconnections at the electron microscopic level. Our study revealed a characteristic distribution of GABAergic and cholinergic elements in the various amygdaloid nuclei: 1) Large, ChAT-immunopositive cells with heavily labeled dendrites were observed in the anterior amygdaloid area and in the lateral and medial zones of the central nucleus. These cells seem to constitute the intraamygdaloid extension of the magnocellular basal nucleus. Their dendrites invaded other amygdaloid nuclei, in particular the intercalated nuclei, the lateral olfactory tract nucleus, and the central zone of the central nucleus. These ChAT-immunoreactive dendrites formed synaptic contacts with GAD-positive terminals. GABAergic terminals probably thus exert an inhibitory amygdaloid influence onto cholinergic neurons of the magnocellular basal nucleus. 2) Two amygdaloid nuclei-the basal dorsal nucleus and the lateral olfactory tract nucleus-contained a dense network of ChAT-immunoreactive fibers and terminals, but they also contained numerous GAD-positive perikarya. Double-immunolabeling experiments revealed cholinergic terminals forming synaptic contacts on GAD-immunopositive cell bodies, dendritic shafts, and spines. 3) The central and medial nucleus seem to be the main target of GABAergic fibers to the amygdala. Both nuclei contained a dense plexus of GAD-immunoreactive terminals that may arise, at least in part, from the GABAergic neurons in the basal dorsal nucleus. Inhibition of the centromedial "excitatory" region through intraamygdaloid GABAergic connections may reduce excitatory amygdaloid influence onto hypothalamus and brainstem.

Amygdala↗
PubMed1985

Ibotenic acid decreases thyrotropin-releasing hormone receptor binding in the rat amygdala.

Thyrotropin-releasing hormone (TRH) receptor densities in the amygdala were examined with quantitative autoradiography in rats treated with the cellular neurotoxin ibotenic acid (IBO). Microinjections of IBO (10 micrograms) into the right basolateral amygdaloid nucleus (BsA) reduced the concentration of TRH receptors in this nucleus by over 50%, when compared to the contralateral BsA and to vehicle-injected control rats. IBO lesions left amygdaloid terminals intact, as shown by normal levels of presynaptic choline uptake sites. Our results strongly suggest that TRH receptors in the amygdala are predominantly located on cell bodies.

Amygdala↗