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 397 records · Page 22Linked to original sources
PubMed1998

[GABA mediated inhibitory effect of amygdala on the activity of medial geniculate body neurons].

On 10 New Zealand white rabbits immobilized with Flaxedil, the inhibitory effect of amygdaloid stimulation on the responses of medial geniculate body (MGB) neurons to tone bursts and the involved neurotransmitter mechanism were investigated with microiontophoresis technique. The results showed that application of GABA could cause a suppression of spontaneous activity of MGB neurons while GABAA antagonist bicuculline had an opposite effect. Iontophoretic injection of GABA gave an inhibitory effect on MGB neurons similar to that caused by stimulating the amygdala or the auditory cortex behind the rhinal sulcus (ACBRS), and in particular, the GABA induced suppression could be completely antagonized by application of bicuculline. Taken together, these data suggested that GABA mediated the amygdaloid inhibitory effect. It seemed unlikely that glycine was involved in the effect, since strychnine, a glycine antagonist, could not affect the descending inhibition from ACBRS area.

Amygdala↗
PubMed1999

Immunohistochemical mapping of enkephalins, NPY, CGRP, and GRP in the cat amygdala.

This immunohistochemical study shows a wide distribution of neuropeptides in the cat amygdala. Neuropeptide Y is present along the whole amygdaloid complex, and fibers and cell bodies containing neuropeptide Y are observed in all the nuclei studied. Leucine-enkephalin-, gastrin-releasing peptide/bombesin-, and calcitonin gene-related peptide-immunoreactive fibers and perikarya are observed only in discrete nuclei of the amygdaloid complex, whereas only fibers -but no cell bodies- containing methionine-enkephalin-Arg6-Gly7-Leu8 have been observed. No immunoreactivity has been found for gamma-melanocyte-stimulating hormone, dynorphin A (1-17), or galanin. These data are compared with those reported in the amygdala of other mammals.

Amygdala↗
PubMed1995

Distribution of neurons of origin of zinc-containing projections in the amygdala of the rat.

The present study describes the distribution of neurons of origin of zinc-containing pathways in the amygdaloid complex of the rat, using the selenium method for simultaneous retrograde labeling of all zinc-containing neurons. With this method, vesicular ionic zinc is precipitated intravitally with selenium compounds and transported retrogradely to the parent neurons, where it can be visualized by silver amplification. Neurons labeled retrogradely with silver-amplified precipitate were observed in all amygdaloid nuclei except for the lateral olfactory tract nucleus, the accessory olfactory tract nucleus and the central nucleus. Very few labeled cell bodies were seen in the anterior amygdaloid area and the medial nucleus. The amygdalo-hippocampal area and the amygdalo-piriform transition area both showed a substantial number of labeled somata throughout their rostrocaudal extent. In the anterior cortical nucleus, very few labeled cell bodies were found in the rostral pole, whereas they were abundant in the caudal quarter of the nucleus. In the posterolateral cortical nucleus, the number of labeled cell bodies increased gradually; there were none in the rostral pole, but most of the neurons in the caudal part were labeled. The posteromedial cortical nucleus contained a great number of labeled somata, but with some variation in the rostrocaudal extent of the nucleus. Considerable numbers of labeled neurons were observed throughout the lateral nucleus. In the basolateral nucleus, a small number of labeled cell bodies was present in the rostral half, but a gradual increase was observed in the caudal direction. Finally, in the basomedial nucleus, very few labeled cell bodies were present in the rostral two-thirds, whilst a considerable number was encountered in the caudal one-third. Possible functional implications of neuronal zinc are considered. The distribution of neurons of origin of zinc-containing projections has been compared with previously described intrinsic connections of the rat amygdala, and tracts that may possibly be zinc-containing are outlined and discussed. It is concluded that in all probability a substantial proportion of the intrinsic connectivity of the rat amygdaloid complex is zinc-containing.

Amygdala↗
PubMed2003

The amygdaloid complex: anatomy and physiology.

A converging body of literature over the last 50 years has implicated the amygdala in assigning emotional significance or value to sensory information. In particular, the amygdala has been shown to be an essential component of the circuitry underlying fear-related responses. Disorders in the processing of fear-related information are likely to be the underlying cause of some anxiety disorders in humans such as posttraumatic stress. The amygdaloid complex is a group of more than 10 nuclei that are located in the midtemporal lobe. These nuclei can be distinguished both on cytoarchitectonic and connectional grounds. Anatomical tract tracing studies have shown that these nuclei have extensive intranuclear and internuclear connections. The afferent and efferent connections of the amygdala have also been mapped in detail, showing that the amygdaloid complex has extensive connections with cortical and subcortical regions. Analysis of fear conditioning in rats has suggested that long-term synaptic plasticity of inputs to the amygdala underlies the acquisition and perhaps storage of the fear memory. In agreement with this proposal, synaptic plasticity has been demonstrated at synapses in the amygdala in both in vitro and in vivo studies. In this review, we examine the anatomical and physiological substrates proposed to underlie amygdala function.

Amygdala↗
PubMed1973

The normalizing effect of lateral amygdalar lesions upon the dorsomedial amygdalar syndrome in dogs.

Two types of bilateral amygdalar lesions were performed successively. The first operation, involving the dorsomedial part, produced aphagia and subsequent hypophagia, vomiting and apathy. Consequently the body weight was reduced. After a few weeks partial recovery occurred. The second operation, involving the lateral part of the amygdaloid complex, produced hyperphagia, increase of body weight and restoration of general arousal. These results indicate the existence of two antagonistic systems: excitatory in the dorsomedial amygdala and inhibitory in the lateral amygdala. Damage of the inhibitory system reverses almost completely the syndrome produced by an initial lesion of the excitatory system.

Amygdala↗
PubMed1994

Effect of electrolytic and chemical lesion by ibotenic acid of the amygdala on salt intake.

Sodium chloride intake was studied in male Holtzman rats weighing 250-300 g submitted to electrolytic and chemical lesion of the cell bodies, not fibers of the amygdaloid complex. Sodium chloride (1.5%) intake increased in animals with electrolytic lesion of the corticomedial nucleus of the amygdala. Sodium chloride (1.5%) intake increased after ibotenic acid injection into the corticomedial nucleus of the amygdala to a larger extent (26.6 +/- 9.2 to 147.6 +/- 34.6 ml/5 days). The results indicate that sodium intake response can be induced by lesions, which involved only cell bodies. The fibers of passage of the corticomedial nucleus of the amygdala produce a water intake less consistent than that induced by ibotenic acid, which is more acute. The results show that cell bodies of this region of the amygdala are involved in the control of sodium chloride intake.

Amygdala↗
PubMed1989

Distribution of somatostatin-like immunoreactivity in the monkey amygdala.

The distribution of somatostatin-like immunoreactivity was studied in the macaque monkey (Macaca fascicularis) by using primary antisera that recognize somatostatin-28 (S309) or somatostatin-28(1-12) (S320). Somatostatin-immunoreactive neuronal cell bodies were observed in all amygdaloid nuclei and cortical regions. The density of labeled cells varied substantially, however, both within and across the various amygdaloid subdivisions. The highest densities of labeled neurons were observed in layer III of the periamygdaloid cortex, in layers II and III of the medial nucleus, in the magnocellular division of the accessory basal nucleus, and in the medial portion of the lateral nucleus. Many labeled cells were also consistently observed in the caudoventral portion of the lateral division of the central nucleus. Labeled cells were heterogeneous in size and shape ranging from small and spherical to large and multipolar. The density of somatostatin-immunoreactive fibers also varied greatly from region to region and was often inversely related to the density of immunoreactive cells. Highest densities of immunoreactive fibers were observed in the periamygdaloid cortex, medial nucleus, parvicellular division of the accessory basal nucleus, paralaminar nucleus, ventrolateral portion of the lateral nucleus, parvicellular division of the basal nucleus, and the lateral division of the central nucleus. Fibers and terminals in the central nucleus had a coarsely varicose appearance and this pattern of staining was continuous along the trajectory of the central nucleus projection to the bed nucleus of the stria terminalis. The large, immunoreactive varicosities located in this area often appeared to outline dendritic or vascular profiles within the substantia innominata. The lowest levels of somatostatin-immunoreactive fibers were observed in the magnocellular division of the basal nucleus and in the ventromedial portion of the accessory basal nucleus.

Amygdala↗
PubMed1998

Neuropeptides in the cat amygdala.

The distribution of seven neuropeptides was studied in the cat amygdala using an indirect immunoperoxidase technique. No labeling was found for luteinizing hormone-releasing hormone or beta-endorphin (1-27). Sparse alpha-melanocyte-stimulating hormone-immunoreactive fibers were found in the basomedial nucleus of the amygdala, whereas a low density of fibers containing alpha-neo-endorphin was observed in the anterior amygdaloid area. Neurotensin was observed in fibers of the anterior amygdaloid area (low density) and both the lateral (low density) and the medial part (moderate density) of the central nucleus. A low density of fibers containing neurokinin A was found in the anterior amygdaloid area, the basolateral nucleus, and the medial part of the central nucleus. A moderate density was observed in the basomedial nucleus and in the medial and cortical nuclei. Fibers containing somatostatin-28 (fragment 1-12) were observed in all the amygdaloid nuclei, whereas immunoreactive cell bodies were found in all the nuclei except in the medial part of the central nucleus and the medial nucleus. Perikarya containing neurokinin A were observed in the latter nucleus. The results point to a discrete distribution of peptidergic fibers in the cat amygdala, as well as the occurrence of neurons containing neurokinin A and somatostatin-28 (fragment 1-12). The distribution of the peptides studied in the cat is compared with the location of the same peptides in the amygdala of other species. The possible diencephalic origin of the peptidergic fibers is also discussed.

Amygdala↗
PubMed2001

The lateral hypothalamus is involved in the pathway mediating the hypotensive response to cingulate cortex-cholinergic stimulation.

1. The injection of acetylcholine (ACh) into the medial prefrontal cortex (MPFC) caused marked hypotensive response in either unanesthetized or anesthetized rats. 2. The present experiment was designed to investigate anatomical connections of the ACh injection site in the MPFC with putative autonomic-related brain nuclei, as well as their possible involvement in the mediation of the hypotensive response to ACh. 3. For the above purpose, the bidirectional neuronal tracer biotinylated dextran amine (BDA) was injected into Cg1 and Cg3 areas, within the MPFC of male Wistar rats. Five days later the animals were sacrificed and brain slices were processed and analyzed to determine neuronal projections efferent from as well afferent to the MPFC. 4. Neuronal staining was more prominent in regions ipsilateral to the BDA injection site. Prominent efferent projections of the MPFC were observed in the contralateral MPFC: ipsi- and contralateral amygdala and hypothalamus; ipsilateral septal area, diagonal band, and zona incerta. 5. Similar but not equal patterns of neuronal labeling were observed when BDA injections were performed within the two adjacent MPFC areas. BDA injections centered in the ACh injection site in the Cg3 area caused strong labeling in the septal area and diagonal band as well as an overall hypothalamic labeling. Within the hypothalamus an intense cortical projection was observed in the lateral hypothalamus (LH). BDA injections into the Cg1 area caused a more evident labeling of the amygdaloid complex. 6. Neuronal cell bodies were evident throughout the MPFC as well as in the sensory-motor cortex when BDA was injected into the LH, thus indicating a massive ipsilateral cortical projection from the Cg3 to the LH. 7. Bilateral NMDA-induced lesions within the LH caused a significant attenuation of the depressor responses to ACh injection in the MPFC, whereas unilateral lesions were marginally effective. These results indicate the involvement of the LH in the mediation of the hypotensive response to ACh injection into the MPFC as well as the bilateral distribution of the hypotensive pathway.

Acetylcholine↗
PubMed1991

Cardiovascular changes induced by chemical stimulation of the amygdala in rats.

The role of the amygdaloid complex in the central regulation of the cardiovascular system was studied in unanesthetized, unrestrained rat. The injection of carbachol into the amygdaloid complex elicited a pressor response, whereas the injection of noradrenaline and 5-hydroxytryptamine into the same area caused no significant cardiovascular changes. The greatest pressor response was obtained when carbachol was injected into the central nucleus. Bradycardia and tachycardia occurred when injection of carbachol was made into dorso-central and medio-ventral parts of the amygdaloid complex, respectively. Concomitant with cardiovascular responses, the injection of carbachol into the amygdaloid complex produced behavioral changes including immobilization, body shaking, searching and rearing. The pressor response and bradycardia were suppressed by prior local injection into the amygdaloid complex of atropine but not hexamethonium. These results suggest that the cholinergic system mediated by activation of muscarinic receptors in the amygdaloid complex may play a role in the control of cardiovascular and autonomic function.

Amygdala↗
PubMed1986

Neuropeptides in the amygdala of controls, schizophrenics and patients suffering from Huntington's chorea: an immunohistochemical study.

The location of the neuropeptides methionine-enkephalin (ME), neurotensin (NT), neuropeptide Y (NPY) and vasoactive intestinal polypeptide (VIP) within the amygdaloid complex of healthy human individuals, schizophrenics and patients suffering from Huntington's chorea was studied qualitatively by means of immunohistochemistry. VIP-like immunoreactivity (IR) was present predominantly in a dense cluster of fibers and terminals in the central amygdaloid nucleus. ME-IR was observed in fibers, terminals and cell bodies in the same subnucleus, exhibiting a characteristical distribution pattern. NT-positive cell bodies were situated within the center of the central amygdaloid nucleus, fibers and terminals being encountered mainly at the periphery. NPY-IR was found to be evenly distributed throughout the amygdala. Distribution and staining intensity of ME, NPY and NT in the amygdala showed no qualitatively recognizable difference between the normal and schizophrenic specimens, whereas VIP-IR appeared to be slightly increased in the central amygdaloid nucleus of schizophrenics. In the choreic cases, the considerably shrunken amygdala exhibited only very low staining intensity of the four investigated neuropeptides.

Adult↗
PubMed1983

Distribution of neuropeptides in the limbic system of the rat: the bed nucleus of the stria terminalis, septum and preoptic area.

The distribution of the neuropeptides vasoactive intestinal polypeptide, cholecystokinin octapeptide, substance P, neurotensin, methionine-enkephalin and somatostatin has been mapped immunocytochemically in the bed nucleus of the stria terminalis, one of the major sites of termination for efferent projections from the amygdala. Immunoreactive fibres and terminals were distributed more or less topographically and largely in accordance with the previously described localization of peptide-containing cell bodies in the amygdala and the amygdaloid projection fields in the bed nucleus as described by neuroanatomical techniques. Thus, vasoactive intestinal polypeptide, which was found in some of the lateral amygdaloid nuclei, had a substantial projection to the lateral bed nucleus. The lateral bed nucleus also contained cholecystokinin-octapeptide, substance P, neurotensin and methionine-enkephalin immunoreactivity which probably derived from the central amygdaloid nucleus, whilst cholecystokinin-octapeptide, and especially substance P-containing fibres, were found in the medial bed nucleus and probably arise from cells in the medial amygdala. Reciprocal amygdalopetal projections were suggested by the presence of substance P- and somatostatin-containing cell bodies in the mediodorsal bed nucleus and vasoactive intestinal polypeptide cells in the lateral bed nucleus, but somatostatin otherwise had a widespread distribution. Numerous local peptidergic connections were also noted both within the bed nucleus and between it and adjacent structures, especially the preoptic area, hypothalamus and the basal ganglia. These data provide further evidence that neuropeptides play a major role in the connectivity of the limbic system and show that the bed nucleus of the stria terminalis is an important relay station, particularly between amygdaloid efferents and other forebrain areas.

Animals↗
PubMed1984

Studies on gustatory responses of amygdaloid neurons in rats.

The responses of 80 amygdaloid neurons to the four basic taste (sucrose, NaCl, HCl and quinine hydrochloride), thermal (5 degrees C, 20 degrees C and 40 degrees C) and tactile (brushing) stimuli applied to the anterior part of the tongue were recorded in anesthetized rats. About 90% of the taste-sensitive amygdaloid neurons responded to thermal and/or tactile stimulations of the tongue as well, and some of them showed convergent responses to tactile stimulation of various parts of the body and to acoustic stimulation. Most (86%) amygdaloid taste-sensitive neurons showed a phasic pattern of excitatory response lasting 1-2 s after onset of stimulation with the broad breadth of tuning to the four taste stimuli. About 35% of the neurons showed monotonic increasing responses with increasing NaCl concentration. The rest of the neurons showed complex intensity-response function. The amygdaloid neurons could be grouped into classes based on their best responsive stimulus, and the response profiles of those neurons showed relative regularity when the four stimuli were hedonically ordered from most to least preferred (i.e., sucrose, NaCl, HCl, quinine). Across-neuron correlations between magnitudes of responses to pairs of the four basic taste stimuli have suggested a tendency that taste information is processed in a hedonic dimension in the amygdala. The neurons in the central (Ce) nucleus showed some differential taste responses from those in other amygdaloid nuclei, i.e., about half of the Ce neurons showed tonic responses, and the across-neuron correlation coefficients in the Ce neurons were much higher than those in the non-Ce neurons.

Amygdala↗
PubMedDate not supplied

Temporal lobe lesion-induced obesity in rats: an anatomical investigation of the posterior amygdala and hippocampal formation.

Bilateral lesions centered in the posterodorsal amygdala of female rats resulted in hyperphagia and excessive weight gain (mean = 65.3 g in 20 days compared to 6.8 g for control animals). The brain damage always extended posteriorly into the ventral hippocampal formation. However, lesions that were confined to the ventral hippocampus or amygdalohippocampal area had no effect on daily food intake or body weight, nor did lesions at any other hippocampal site. In a previous study, lesions of the basolateral, corticomedial, and anterior groups of amygdaloid nuclei failed to affect food intake or body weight. It is concluded that the posterodorsal aspect of the amygdala is the critical site for this experimentally induced obesity syndrome. New coordinates for the effective site are presented.

Amygdala↗
PubMed2004

Distribution of zincergic neurons in the mouse forebrain.

Synaptically released zinc is thought to play an important role in neuronal signaling by modulating excitatory and inhibitory receptors and intracellular signaling proteins. Consequently, neurons that release zinc have been implicated in synaptic plasticity underlying learning and memory as well as neuropathological processes such as epilepsy, stroke, and Alzheimer's disease. To characterize the distribution of these neurons, investigators have relied on a technique that involves the retrograde transport of zinc-selenium crystals from axonal boutons to the cell bodies of origin. However, one major problem with this method is that labeling of cell bodies is obscured by high levels of staining in synaptic boutons, particularly within forebrain structures where this staining is most intense. Here, we used a modification of the retrograde labeling method that eliminates terminal staining for zinc, thereby enabling a clear and comprehensive description of these neurons. Zincergic neurons were found in all cerebral cortical regions and were arranged in a distinct laminar pattern, restricted to layers 2/3, 5, and 6 with no labeling in layer 4. In the hippocampus, labeling was present in CA1, CA3, and the dentate gyrus but not in CA2. Labeled cell bodies were also observed in most amygdaloid nuclei, anterior olfactory nuclei, claustrum, tenia tecta, endopiriform region, lateral ventricle, lateral septum, zona incerta, superior colliculus, and periaqueductal gray. Moreover, retrograde labeling was also noted in the dorsomedial and lateral hypothalamus, regions that previously were thought to be devoid of neurons with a zincergic phenotype. Collectively these data show that zincergic neurons comprise a large population of neurons in the murine forebrain and will provide an anatomical framework for understanding the functional importance of these neurons in the mammalian brain.

Animals↗
PubMed1995

Vasopressin in the brain of a desert hibernator, the jerboa (Jaculus orientalis): presence of sexual dimorphism and seasonal variation.

The distribution of vasopressin innervation in the brain of the jerboa (Jaculus orientalis) was investigated, with special attention to sex differences and seasonal variations. Vasopressin perikarya were observed in the paraventricular and supraoptic nuclei, the suprachiasmatic nucleus, the periventricular nucleus, the medial preoptic area, the bed nucleus of the stria terminalis, and the medial amygdaloid nucleus. In addition, vasopressin cell bodies were observed in the ventral retrochiasmatic area. After treatment with colchicine, vasopressin perikarya were also observed around the organum vasculosum laminae terminalis, in the medial diagonal band of Broca, and in the dorsal medial preoptic nucleus. Vasopressin fibers were also found to be more widespread in the jerboa brain than in other rodents. Fibers were observed in the medial diagonal band of Broca, the stria medullaris, the tuber cinerum, the area postrema, the medial vestibular nucleus, and the dorsal motor nucleus of the vagus. Sexual dimorphism and seasonal variation in vasopressin immunoreactivity were observed in areas that not only showed a testosterone-dependent vasopressin innervation in other rodents but also in the paratenial and mediodorsal thalamic nuclei, the tuber cinerum, the supramammillary complex, the zona incerta, the interpeduncular complex, and the dorsal and medial raphe nuclei. A denser vasopressin innervation was observed in spring/summer (sexual active period) than in autumn. Numerous brain structures contained vasopressin receptors (cerebral cortex, hypothalamus, substantia nigra, dentate gyrus, thalamic nuclei, superior colliculus, dorsal cochlear nucleus, and cerebellum); no sex- or season-related differences were observed. These data indicate a high level of vasopressin in the jerboa brain, which may reflect an adaptation to its harsh bioclimatic environment.

Adaptation, Physiological↗
PubMed1993

Differential effects of excitotoxic lesions of the amygdala on cocaine-induced conditioned locomotion and conditioned place preference.

The reinforcing properties of cocaine can readily become associated with salient environmental stimuli that acquire secondary reinforcing properties. This type of classical conditioning is of considerable clinical relevance, as intense drug craving can be evoked by the presentation of stimuli previously associated with the effects of cocaine. Given the large body of evidence that implicates the amygdaloid complex in the learning of stimulus-reward associations, the present experiments examined the effects of quinolinic acid lesions of the amygdala on cocaine-induced conditional locomotion and conditioned place preference (CPP). Destruction of the amygdala did not affect basal or cocaine-induced locomotion, suggesting that the amygdala does not mediate the unconditioned psychomotor stimulant effects of this drug. Preconditioning lesions also failed to affect cocaine-induced conditional locomotion. Specifically, exposure of both lesioned and non-lesioned rats to a cocaine-paired environment produced significant conditional increases in locomotion. This lack of effect was contrasted by a complete blockade of cocaine-induced CPP by the amygdaloid lesions. These data demonstrate that cocaine-induced stimulus-reward conditioning can be differentially affected by lesions of the amygdala.

Amygdala↗
PubMed1984

Distribution of immunoreactive dynorphin A1-8 in discrete nuclei of the rat brain: comparison with dynorphin A.

The distribution of immunoreactive (ir)-dynorphin A1-8 (Dyn A1-8) in 78 microdissected rat brain areas as well as in the neurointermediate lobe of pituitary gland was determined using a highly specific radioimmunoassay. The highest concentrations of Dyn A1-8 in brain were found in substantia nigra (673.8 fmol/mg protein) and lateral preoptic area (565.1 fmol/mg protein). High concentrations of ir-Dyn A1-8 (greater than 240 fmol/mg protein) were found in 5 nuclei: ventral premamillary nucleus, anterior hypothalamic nucleus, dorsomedial nucleus, arcuate nucleus, and medullary reticular nuclei. Moderate concentrations of the peptide (between 120 and 240 fmol/mg protein) were found in 55 brain nuclei such as septal and amygdaloid nuclei, most diencephalic structures, mesencephalic nuclei, pons and medulla oblongata nuclei and others. Low concentrations of ir-Dyn A1-8 (less than 120 fmol/mg protein) were found in 16 regions, e.g. frontal cortex, hippocampus, caudate-putamen cortical amygdaloid nucleus, several thalamic nuclei, mamillary body superior and inferior colliculi, cerebellar nuclei and others. The posterior thalamic nucleus has the lowest ir-Dyn A1-8 concentration (62.0 fmol/mg protein). The neurointermediate lobe of the pituitary gland is extremely rich in ir-Dyn A1-8 (4063.0 fmol/mg protein).

Animals↗