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PubMed1983

Corticotropin releasing factor: immunocytochemical localization in rat brain.

Using antiserum generated against the synthetic CRF1-41 we have immunocytochemically localized perikarya and processes in rat brain. Areas observed to have particularly dense accumulation of CRF-ir cells were in the extra-hypothalamic areas of nucleus accumbens septi, nucleus of the stria terminalis, the medial preoptic region, and the central amygdaloid nucleus. Within the hypothalamus cell bodies were scattered throughout the anterior hypothalamic region and densely packed in the paraventricular nucleus. Fibers appear most dense in the lateral septal region and throughout the external layer of the median eminence.

Afferent Pathways↗
PubMed1992

N-methyl-D-aspartate lesions of the lateral and basolateral nuclei of the amygdala block fear-potentiated startle and shock sensitization of startle.

Cell bodies in the lateral and basolateral amygdaloid nuclei were destroyed by local infusion of N-methyl-D-aspartate. Adjacent areas, such as the central amygdaloid nucleus, were largely spared. Lesions were carried out before training and testing (Experiment 1) or after training but before testing (Experiment 2). In both cases, the lesions completely blocked fear-potentiated startle (increased acoustic startle in the presence of a light previously paired with footshock). They also blocked increased startle after a series of footshocks, provided they damaged the most anterior part of the basolateral nucleus. It is suggested that the lateral or basolateral amygdaloid nuclei (or both) relay visual information to the central amygdaloid nucleus, which is also critical for fear-potentiated startle. In addition, activation of the most anterior part of the basolateral nucleus may be critical for processing shock information during fear conditioning.

Amygdala↗
PubMedDate not supplied

Feeding and body weight regulation after 6-OHDA application into the preoptic area.

Our previous results showed that neurochemical destruction of the amygdaloid terminal field of the mesolimbic dopaminergic system caused disturbances in body weight regulation and feeding. In the present experiments, it was studied whether 6-hydroxydopamine (6-OHDA)-induced bilateral lesions of the mesolimbic dopaminergic system in the lateral preoptic area produce similar symptoms in rats. To enhance the selectivity of the neurotoxin, 6-OHDA was also used after desmethylimipramine (DMI) premedication. Both 6-OHDA and 6-OHDA + DMI treatments resulted in hypophagia, hypodipsia and body weight decrease. A significant increase of water intake was found in sham-operated controls and lesioned animals, in response to extracellular dehydration caused by polyethylene glycol. Intracellular dehydration induced by hypertonic saline resulted in increase of water intake of all animals; however, 6-OHDA- and 6-OHDA + DMI-treated rats drank less than the controls. Similar observation has been made when food intakes were compared after 2-deoxy-D-glucose treatment. Results show that mesolimbic dopaminergic elements play an essential role in the regulation of feeding.

Animals↗
PubMed1985

The vasopressinergic innervation of the brain in normal and castrated rats.

A detailed description is given of the distribution of vasopressin-immunoreactive structures in the brain of intact adult male rats. By application of a modified immunocytochemical procedure, vasopressin-immunoreactive fibers were detected in many new areas. In adult male rats which were castrated 15 weeks before death, vasopressin-immunoreactive cell bodies had disappeared from the bed nucleus of the stria terminalis and the medial amygdaloid nucleus. No obvious changes were found in vasopressin-immunoreactive cell bodies in other areas. Furthermore, a very strong reduction was seen in the density of vasopressin-immunoreactive fibers in the olfactory tubercle, nucleus of the diagonal band and its immediate surroundings, ventral pallidum, basal nucleus of Meynert, lateral septum, septofimbrial nucleus, ventral hippocampal formation, amygdaloid area, pre- and supramammillary nucleus, supramammillary decussation, (inter)dorsomedial, parafascicular, and ventral aspect of paraventricular thalamic nuclei, zona incerta, lateral habenular nucleus, ventral tegmental area, substantia nigra, periventricular gray, dorsal and median raphe nucleus, and locus coeruleus. No changes were observed in other areas containing vasopressin-immunoreactive fibers. These changes following gonadectomy were not observed in castrated rats which had been treated with testosterone. The results suggest that vasopressin projections from the bed nucleus of the stria terminalis and possibly from the medial amygdaloid nucleus require the presence of gonadal hormones for their normal appearance. This is in contrast to pathways arising from the hypothalamic vasopressin-producing nuclei, which fail to show obvious changes following castration.

Animals↗
PubMed1975

Effect of amygaloid lesions on gonadal maturation in male and female ferrets.

Two experiments were performed to determine whether the amygdala is involved in theregulation of gonadal maturation in the ferret. In an experiment with prepuberal males it was found that testicular and epididymal wieghts, seminiferous tubule diameters, Leydid cell number, and ratings of spermatogenic development were the samein animals autopsied 4 wk after either the placement of a platinum-elctrode lesion in the amygdala or a sham operation. Testosterone concentrations both in testis and in blood tended to be lower, and body growth was significantly retarded in males with amygdaloid lesions. In a second experiment with prepuberal females it was found that the first estrus occurred significantly earlier in ferrets that had received amygdaloidlesions than in sham-operated controls. Neither body growth nor fertility of femaleswas affected. These findings suggest that the amygdala exerts an inhibitory influence on the hypothalamic mechanism which controls the secretion of gonadotropins required for initial estrus in female ferrets, but not for the initail masturation of the testes in males.

Amygdala↗
PubMed1984

Role of the visceral brain in body equilibrium.

A series of examinations were carried out to determine whether the limbic system, particularly the hippocampus and the amygdaloid nucleus, participates in the production of disequilibrium of the eyes and the body and to clarify the conditions which induce disequilibrium. Over-stimulation of the rabbit's hippocampus induces over-excitation of adrenergic components involved in this part of the brain, through which dysfunction of equilibrium center in the brain stem is eventually brought about. This dysfunction leads to disequilibrium of the eyes and the body. On the basis of these results, equilibrium tests for neurotic vertigo were devised. Using these equilibrium tests we noted that in a certain group of traumatized patients who suffer from vertigo of psychosomatic origin, there are two etiological factors: functional linkage between the temporal cortex and the limbic system, particularly the hippocampus in regard to a memory or a conditioned reflex relevant to vertigo, over-excitation of the adrenergic components involved in the brain connecting the hippocampus, the hypothalamus and equilibrium centers in the brain stem. These two etiological factors induce disequilibrium by a trigger-and-target relationship in which the former acts as a trigger and the latter as a target. The cerebellum is not an essential factor in producing vertigo of psychosomatic origin, but it enhances vertigo of this type through activation of the adrenergic components, particularly those in the hippocampus. Thus, in patients with both vertigo of psychosomatic origin and cerebellar symptoms recovery from vertigo tends to be delayed. Over-stimulation of the rabbit's amygdaloid nucleus, particularly its medial portion and the habenular nucleus induces over-excitation of adrenergic components involved in these parts of the brain. These animals develop disequilibrium of the eyes in response to an olfactory stimulus, such as extract of garlic. On the basis of these results, equilibrium tests for olfactory vertigo were devised. Using these equilibrium tests we noted that traumatized patients who suffered from vertigo due to inhalation of garlic vapor showed hyper-reactivity to adrenaline and developed disequilibrium of the eyes and the body when given a subcutaneous injection of this drug. These findings indicate that olfactory vertigo is induced by a mechanism in which olfactory stimulation affects the above adrenergic components, causing disequilibrium of the eyes and the body.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed2004

Contribution of the medial amygdaloid nucleus to the development of hypertension in spontaneously hypertensive rats.

We previously demonstrated involvement of the medial amygdaloid nucleus in restraint stress-induced pressor responses in rats. In this study, neuronal perikarya in the medial amygdaloid nucleus of 4-week-old spontaneously hypertensive rats (SHR) were selectively destroyed with ibotenic acid. Bilateral lesions of the medial amygdaloid nucleus attenuated the development of hypertension in SHR. Body weight gain was not different between lesioned and sham-lesioned SHR throughout the experimental periods. These data suggest that neurons in the medial amygdaloid nucleus may be involved in the development of hypertension in SHR.

Amygdala↗
PubMed2000

An anterograde and retrograde tract-tracing study on the projections from the thalamic gustatory area in the rat: distribution of neurons projecting to the insular cortex and amygdaloid complex.

Projections from the thalamic gustatory nucleus, i.e. the parvicellular part of the posteromedial ventral thalamic nucleus (VPMpc) to the forebrain regions were studied in the rat by the tract-tracing methods with anterograde tracer (biotinylated dextran amine, BDA) and anterograde/retrograde tracer (wheat-germ agglutinin-horseradish peroxidase, WGA-HRP). After BDA injection into the VPMpc, terminal labeling was observed in the insular cortex, amygdaloid complex, and fundus striati. The terminal labeling in the amygdaloid complex was distributed in dorsolateral area of the rostral part of the lateral amygdaloid nucleus and the rostral part of the lateral subdivision of the central amygdaloid nucleus. The terminal labeling in the central amygdaloid nucleus extended to the fundus striati. The retrograde tracing study with WGA-HRP revealed that the projection fibers from the VPMpc to the amygdaloid complex originated from the medial part of the VPMpc and also from the thalamic area medial to the VPMpc. In the rats injected with Fluoro-Gold and WGA-HRP, respectively into the insular cortex and amygdaloid complex, no double-labeled neuronal cell bodies were found in the VPMpc, although neurons labeled singly with Fluoro-Gold were intermingled with those singly labeled with WGA-HRP in the medial part of the VPMpc. The results indicated that VPMpc neurons projecting to the amygdaloid complex constituted a population different from VPMpc neurons projecting to the insular cortex.

Amygdala↗
PubMed1996

Distribution of pituitary adenylate cyclase activating polypeptide (PACAP) immunoreactivity in the hypothalamus and extended amygdala of the rat.

Pituitary adenylate cyclase activating polypeptide (PACAP) is found in two forms of 27 and 38 amino acids (PACAP-27 and PACAP-38 respectively) in the mammalian central nervous system. Using antibodies to these two forms of PACAP, we examined the distribution of PACAP immunoreactivity in the rat hypothalamus and a number of extrahypothalamic areas. The patterns of immunostaining for PACAP-27 and PACAP-38 were similar: prominent terminal labelling was present in the retrochiasmatic area, median eminence, and posterior periventricular nucleus of the hypothalamus as well as the bed nucleus of the stria terminalis and amygdaloid complex. After colchicine treatment, immunopositive cell bodies were found in the preoptic region of the periventricular zone of the hypothalamus, the suprachiasmatic and paraventricular hypothalamic nuclei, neural structures adjacent to the median eminence (including the retrochiasmatic area, arcuate nucleus, ventromedial hypothalamus, and tuber cinereum), and the lateral mammillary and supramammillary nuclei. In all these areas, immunolabelling appeared specific since it was abolished by preabsorption of primary antisera with the appropriate PACAP peptide. However, the number of immunopositive cells in the suprachiasmatic nucleus was also reduced by preabsorption of PACAP-27/38 antisera with vasoactive intestinal polypeptide, suggesting that a subpopulation of cells in the suprachiasmatic nucleus express a peptide which has significant sequence homology with both PACAP-27/38 and vasoactive intestinal polypeptide. The distribution of PACAP immunoreactivity throughout the hypothalamus, bed nucleus of the stria terminalis, and amygdala suggests the involvement of PACAP in a number of processes including limbic, autonomic, and neuroendocrine functions as well as regulation of the circadian pacemaker.

Amygdala↗
PubMed2001

Localization of neurotensin NTS2 receptors in rat brain, using.

The brain localization of the neurotensin receptor NTS2 was studied with [3H]levocabastine, using an autoradiographic procedure. This study suggests that NTS2 receptors are mainly intracellular. High densities of binding sites were observed in the cingulate, insular, temporal, occipital, enthorhinal cortex, amygdaloid complex, septohippocampal nuclei, medial thalamus, mammillary bodies and superior colliculi; a moderate labelling was observed in the anterior and medial hippocampus, olfactory tubercle, hypothalamus, periaqueductal gray matter, caudate putamen, nucleus accumbens, septum, lateral thalamus, dorsal raphe nucleus and cerebellum; finally, a low labelling was apparent in the ventral tegmentum area and substantia nigra. Thus it appears that NTS2 receptors are particularly abundant in the cerebral cortex, the limbic areas and some areas involved in pain perception.

Animals↗
PubMed1998

Double dissociation of the behavioural effects of R(+) 7-OH-DPAT infusions in the central and basolateral amygdala nuclei upon Pavlovian and instrumental conditioned appetitive behaviours.

Dopaminergic cell bodies located within the ventral mesencephalon innervate the amygdaloid complex, a region critically involved in the attribution of affective significance to environmental stimuli. Recently, we have shown that post-session intra-amygdala administration of a D3 dopamine receptor agonist enhances selectively the acquisition of an appetitive conditioned response. In the present study, we have investigated the potential involvement of the central nucleus and the basolateral nuclei of the amygdala in mediating this effect. Thus, rats were trained to associate an arbitrary stimulus (CS+) with the availability of 10% sucrose reward. Post-session infusions of the D3 receptor-preferring agonist, R(+) 7-OH-DPAT, were made into either the central nucleus or basolateral nuclei. Acquisition of a conditioned approach response was enhanced by R(+) 7-OH-DPAT infusions within the central nucleus, but not within the basolateral nuclei. Drug infusions into either region failed to affect approach behaviour elicited by presentation of a control stimulus (CS-), explicitly unpaired with sucrose reward. The effects of pre-test infusions of R(+) 7-OH-DPAT on the instrumental properties of the stimuli were then determined. Rats were presented with two novel levers, depression of one lever resulted in presentation of the CS+, while presentation of the CS- was contingent upon depression of the other lever. Rates of response upon each lever as well as the ability of the conditioned stimuli subsequently to elicit conditioned approach behaviour were recorded. Data revealed a double dissociation of the effects of R(+) 7-OH-DPAT on the expression of the Pavlovian and instrumental properties of the reward-related stimulus. Thus, within the central nucleus R(+) 7-OH-DPAT dose-dependently attenuated expression of the conditioned approach response, but had no effect upon instrumental responding maintained by the conditioned reward. In contrast, within the basolateral nuclei, R(+) 7-OH-DPAT had no effect upon expression of conditioned approach behaviour, but abolished selectively the ability of the reward-associated stimulus to support the acquisition of a novel instrumental response. Hence, these data indicate that distinct regions of the amygdaloid complex process distinct aspects of conditioned appetitive behaviours.

Amygdala↗
PubMed1996

Enhancements in swim stress-induced hypothermia, but not analgesia, following amygdala lesions in rats.

Lesions placed in the rat amygdala significantly reduce analgesic responses induced either by conditioning or exposure to a cat. Such lesions have alternatively reduced or failed to affect unconditioned foot shock analgesia. The present study expanded the situational determinants by examining whether lesions placed in the amygdala altered analgesia or hypothermia elicited by exposure to either continuous (CCWS) or intermittent (ICWS) cold-water swims. Lesion extent included the central, medial cortico-medial, baso-lateral, baso-medial and lateral amygdaloid nuclei. Basal jump thresholds, but not core body temperatures were significantly increased by unilateral and bilateral amygdala lesions. In contrast, the hypothermic, but not the analgesic responses following CCWS and ICWS were significantly enhanced by unilateral and bilateral amygdala lesions. These data support a hypothesis suggesting that these lesions are effective in reducing those classes of analgesic responses related to the signals of stressors than to the stressors themselves.

Amygdala↗
PubMed1990

Postnatal development of striatal connections in the rat: a transport study with wheat germ agglutinin-horseradish peroxidase.

This paper deals with the postnatal development of afferent and efferent connections of the rat striatum as revealed by the transport of horseradish peroxidase conjugated with wheat germ agglutinin (WGA-HRP). Tracer was injected weekly from birth to the end of the first postnatal month in the head of the caudate nucleus. To control for transport from cortical areas contaminated by the micropipette, injections in newborn rats were made by either vertical or lateral penetrations. In addition some newborn and 14-day-old animals were injected only in the cortex. The results showed that at birth there was retrograde transport to the thalamus, substantia nigra and raphe nuclei. Labelling in the cortex was seen at birth but was probably due to cortical contamination. Transport from the striatum was clearly established on day 7, when a few labelled neurons were observed on both the ipsi and contralateral sides. These neurons increased in number and were distributed through layers III to VI by day 14. At this time labelled cell bodies were observed in the claustrum and lateral amygdaloid nucleus as well as in the globus pallidus and entopeduncular nucleus. On day 21 the contralateral labelling of the lateral amygdaloid nucleus was apparent. The anterograde transport from the striatum to globus pallidus, entopeduncular nucleus and substantia nigra was already visible at birth although its intensity increased during the first postnatal month.

Aging↗
PubMed1992

The GABAA receptor gamma 1 subunit is expressed by distinct neuronal populations.

The distribution of GABAA receptor gamma 1 subunit was examined in the rat central nervous system using in situ hybridization histochemistry. The gamma 1 subunit was expressed in relatively limited areas compared to other subunits investigated previously. The brain regions strongly expressing this subunit were the septum, globus pallidus, bed nucleus of the stria terminalis, hypothalamic periventricular nucleus, supraoptic nucleus, medial and central nuclei of the amygdaloid complex, medial part of the medial geniculate body, substantia nigra pars reticulata, interpeduncular nucleus, lateral parabrachial nucleus, Purkinje cell layer of the cerebellum, and inferior olivary nucleus. This relatively limited expression implies a possible role of gamma 1 subunit in relation to some specific neuronal circuit.

Animals↗
PubMed1992

Organization of amygdaloid projections to brainstem dopaminergic, noradrenergic, and adrenergic cell groups in the rat.

The distribution of amygdaloid axons in the various brainstem dopaminergic, noradrenergic, and adrenergic cell groups was examined. This was accomplished by means of the Phaseolus vulgaris leucoagglutinin lectin (PHA-L) anterograde tracing technique combined with glucose-oxidase immunocytochemistry to catecholamine markers (i.e., tyrosine hydroxylase, dopamine beta hydroxylase, and phenylethanolamine N-methyltransferase). Injections of PHA-L in the medial part of the central amygdaloid nucleus resulted in axonal and terminal labeling in most catecholamine cell groups in the brainstem. Amygdaloid terminals appeared to contract catecholaminergic cells in several brainstem regions. The most heavily innervated catecholaminergic cells were the A9 (lateral) and A8 dopaminergic cell groups and the C2/A2 adrenergic/noradrenergic cell groups in the nucleus of the solitary tract. The medial part of the A9 and adjacent A10 dopaminergic cell groups was moderately innervated. A moderate innervation by amygdaloid terminals was observed on rostral locus coeruleus noradrenergic cells (A6 rostral) and adrenergic cells of the rostral ventrolateral medulla (C1). Noradrenergic cells of the A5, main body of the locus coeruleus (A6), A7, and subcoeruleus were sparsely innervated. Amygdaloid axons were not observed on noradrenergic neurons of the A4 cell group, area postrema, and A1 cells of the ventrolateral medulla. The results demonstrate that the amygdala primarily innervates the dopaminergic cells of midbrain (i.e., A8 and lateral A9 cells) and the adrenergic cells (C2) and noradrenergic (A2) cells in the nucleus of the solitary tract. The possible functional significance of amygdaloid innervation of catecholaminergic cells is discussed.

Amygdala↗
PubMed1988

Distribution of cholecystokinin-immunoreactive cell bodies in the male and female rat: II. Bed nucleus of the stria terminalis and amygdala.

The distribution of cholecystokinin-immunoreactive (CCK-I) cell bodies was studied in the bed nucleus of the stria terminalis (BST) and amygdaloid complex of colchicine-treated male and female rats. Immunoreactive cells were visualized in the BST medial amygdaloid (MeA), central lateral, basolateral, basolateral ventral, medial, intercalated, anterior cortical, and posterior cortical nuclei and the amygdalohippocampal zone. Several significant sex differences were observed. In the male, a dense aggregation of CCK-I cell bodies was visualized in the MeA, especially in the dorsocaudal part and in the encapsulated part of the BST. In comparison, female rats had relatively fewer immunoreactive cells in both of these regions. In the lateral and basolateral amygdaloid nuclei, however, more CCK-I cells were visualized in the female than in the male, but the difference was not statistically significant. These data provide characterization of a sexually differentiated CCK system. In addition, we observed that the number of CCK-I cells in the BST and posterodorsal part of the MeA was substantially reduced after castration. The number of CCK-I cells in female rats, however, was not significantly reduced after ovariectomy in any of the regions studied. These findings imply that the steroid regulation of CCK is sexually differentiated. The sexually dimorphic distribution of CCK-I cells in areas that are targets of steroid hormones and regulate reproductive processes is consistent with the possibility that CCK participates in central integration of sensory and steroidal input that modulates reproductive behavior.

Amygdala↗
PubMed1994

Distribution of vesicular stomatitis virus proteins in the brains of BALB/c mice following intranasal inoculation: an immunohistochemical analysis.

Earlier studies have shown that intranasal instillation of vesicular stomatitis virus (VSV), a negative-sense RNA virus, in mice and rats can result in infection of the brain, hind-limb paralysis and death. Using an antiserum directed against VSV proteins, we sought to determine the potential neuronal and non-neuronal pathways VSV utilize, for central nervous system dissemination in BALB/c mice. Within 12 h following intranasal inoculation of VSV, VSV antigen could be detected in the olfactory nerve layer of the ipsilateral olfactory bulb. Within 3-4 days post-inoculation (p.i.), VSV had disseminated into the glomeruli of the olfactory bulb as well as the anterior olfactory nuclei that were ipsilateral to the VSV instillation. Within the glomeruli, VSV antigen was more prevalent in the granule cells than in the mitral cells. Correspondingly, the lateral olfactory tract, where axons of mitral cells course, remained VSV negative throughout 7 days p.i. By 7 days p.i., viral proteins were detected in several additional regions extending to the brainstem. These included regions involved in theta-rhythm generation during exploration and REM sleep, i.e. the septal nuclei, the supramammillary body, and the hippocampal formation, as well as the amygdaloid complex and brainstem neuromodulatory centers, such as the dorsal raphé and locus coeruleus. Structures abutting the ventricular surfaces, such as the dorsal cochlear nucleus, were also labeled. Tracts immunoreactive to VSV included the dorsal tegmental tract, fascia retroflexus, Probst tract, and mesencephalic tract of the trigeminal motor nerve. Besides the lateral olfactory tract, tracts that remained VSV negative included the anterior commissure, the corpus callosum and the mammillary peduncle. The pattern of VSV immunoreactivity supports the idea that following infection of the olfactory bulb glomeruli, VSV spreads via both ventricular surfaces and retrograde transport within axons of neuromodulatory transmitter systems innervating the olfactory bulb. Conversely, regions exhibiting low levels of VSV antigen are not likely to be involved in VSV dissemination. In particular, the paucity of VSV antigen in some of the terminal fields of neuromodulatory systems indicate that anterograde transport is more selective than retrograde transport. Surprisingly, the principal neurons of the olfactory glomeruli, thalamus, cerebral cortex and the hippocampus, all of which use L-glutamate as the excitatory neurotransmitter, are much less involved in viral dissemination.

Administration, Intranasal↗