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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↗

PubMed1986

Development of the lateral amygdaloid nucleus in the human fetus: transient presence of discrete cytoarchitectonic units.

The cytoarchitectonic development of the lateral amygdaloid nucleus has been studied on Nissl-stained sections through brains of human fetuses ranging between 11 to 24 weeks of gestation. The first sign of cytoarchitectonic inhomogeneity of the lateral amygdaloid nucleus is the appearance of 2-3 ovoid cell clusters around 12 weeks of gestation. Between 12.5-16 weeks of gestation, the ventral part of the lateral amygdaloid nucleus contains 7-11 columnar cell clusters separated by "septa" of lower cell-packing density. These columnar clusters, stretching in the rostrocaudal direction, appear on cross-section as ovoid structures elongated in the ventrodorsal direction. In subsequent development (16-24 weeks of gestation) this distinct columnar appearance becomes less obvious, owing to the disappearance of "septa" along the dorsal edges of cellular clusters. This process begins first in the medial part of the columnar field. As a result, the cytoarchitectonic units gradually fuse into a homogeneous grey mass. However, the ventral part of the columnar field retains an undulated appearance throughout late gestation, showing multiple indentations as a sign of former cytoarchitectonic inhomogeneities. In conclusion, the fetal lateral amygdaloid nucleus contains a number of cytoarchitectonic "moduli" which could serve as a new parameter for an estimation of histogenetic maturity of the human amygdala. This transient cytoarchitectonic inhomogeneity could be a sign of the temporary predominance of one characteristic afferent-efferent system during a given developmental stage. Alternatively, it could reflect a clustered type of neurogenesis.

Amygdala↗

PubMed1995

Neuroanatomical and functional specificity of the basolateral amygdaloid nucleus in taste-potentiated odor aversion.

The present study aimed at documenting the neurobiological substrate of taste-potentiated odor aversion (TPOA) in the rat. The role of several temporal lobe structures in discriminative TPOA learning was questioned. The effects of excitotoxic lesions (ibotenate) of the basolateral amygdaloid nucleus, the central amygdaloid nucleus, the caudate putamen nucleus, and aspirative lesion of the entorhinal cortex were studied. The results show that only basolateral amygdaloid nucleus (ABL) damage impaired TPOA. This effect was selective of TPOA, since it spared conditioned taste aversion (CTA) and olfactory perception. In order to find out which process in TPOA requires normal functioning of the ABL, the effects of microinjections of a GABAA agonist (muscimol) into the ABL at various stages of the experiment were examined. The results show that application of muscimol during the acquisition, before or after the presentation of the odor-taste stimulus, impaired TPOA without affecting CTA. Contrastingly, application of muscimol before the test impaired neither TPOA nor CTA. These results suggest that ABL is involved in the acquisition but not in the retrieval of TPOA. The efficacy of muscimol microinjected after the presentation of the odor-taste stimulus further suggests that the deficit is not due to a sensory impairment but rather to the disruption of a memory process, critical for TPOA.

Amygdala↗

PubMed1990

Serotonin-, substance P- or leucine-enkephalin-containing neurons in the midbrain periaqueductal gray and nucleus raphe dorsalis send projection fibers to the central amygdaloid nucleus in the rat.

By a double-labeling method combining the retrograde tracing of horseradish peroxidase and the immunocytochemical technique, serotonin-, substance P- or leucine-enkephalin-like immunoreactive neurons in the midbrain periaqueductal gray (PAG) and the nucleus raphe dorsalis (DR) of the rat were found to send projection fibers to the central amygdaloid nucleus bilaterally with an ipsilateral dominance. These PAG neurons were chiefly distributed in the ventrolateral PAG subdivision and the ventral parts of medial PAG subdivision at the middle and caudal levels of PAG.

Amygdala↗

PubMed1992

Colocalization of peptide- and tyrosine hydroxylase-like immunoreactivities with Fos-immunoreactive neurons in rat central amygdaloid nucleus after immobilization stress.

The central amygdaloid nucleus (ACe) is part of the amygdaloid body, and it has been shown to participate in several stress related reactions. The ACe is densely innervated by tyrosine hydroxylase- (TH), corticotropin releasing factor- (CRF), calcitonin gene-related peptide- (CGRP), neurotensin- (NT), somatostatin- (SOM), enkephalin- (ENK), substance P- (SP), vasoactive intestinal polypeptide- (VIP) and cholecystokinin- (CCK) immunoreactive (IR) nerve terminals. In addition, the ACe contains numerous CRF-, NT-, SOM-, ENK- and SP-IR perikarya. In previous studies it has been shown that stress stimulates the expression of the immediate early gene c-fos in the ACe. The aim of this study was to demonstrate the colocalization of the Fos-IR neurons with the peptide- and TH-IR structures using an immunocytochemical double staining technique. In intact animals the ACe contained only a few Fos-IR neurons. After immobilization stress about 100 Fos-IR neurons were seen per section. They were mainly located in the area, which was enriched by peptide- and TH-IR nerve terminals. The close contacts observed between the Fos-IR neurons and the peptide- and TH-IR nerve endings suggest that the Fos-IR neurons were innervated by these nerve terminals. Furthermore, several NT-, ENK-, SOM- and CRF-IR neurons were observed and the vast majority of these cells exhibited Fos-like immunoreactivity. These results suggest that stress enhances the synaptic activity of the ACe, which stimulates the expression of c-fos. Subsequently, Fos may regulate the expression of the NT, ENK, SOM and CRF genes and thus affect the peptidergic efferents from the ACe.

Amygdala↗

PubMed2004

[Changes of neuronal nitric oxide synthase-immunopositive neurons in the central amygdaloid nucleus of spontaneously hypertensive rats].

OBJECTIVE: To observe the changes of neuronal nitric oxide synthase (nNOS)-immunopositive neurons in the central amygdaloid nucleus of spontaneously hypertensive rats (SHRs). METHODS: Thirty SHRs and 30 Wistar-Koyto rats (WKYs) were sacrificed at the ages of 90, 180, and 360 days respectively to observe the changes of nNOS-immunopositive neurons with ABC immunocytochemical assay. RESULTS: No significant changes were observed in the blood pressure of WKY rats at the specified time points, when SHRs maintained significantly higher blood pressures from 20.8+/-1.1 and 26.3+/-1.0 kPa (P<0.05), gradually increasing during the development of hypertension. The nNOS-immunopositive neurons in the central amygdaloid nucleus were of moderate sizes with long intersected nerve fibers. No significant changes were found in WKY rats. The number of the positive neurons decreased with age in SHRs, especially obvious at 360 days (P<0.05), which was significantly different from that in the WKYs (P<0.05). CONCLUSION: The reduction of nNOS-immunopositive neurons in the central amygdaloid nucleus of SHRs might accelerate the development of hypertension by modulating the cardiovascular function and sensory transmission.

Age Factors↗

PubMed1991

Selective reduction of glucocorticoid receptor immunoreactivity in the hippocampal formation and central amygdaloid nucleus of the aged rat.

Hippocampal cell loss during aging has been related to the toxic effects of corticosterone on this cell population. It is not known which receptor mediates corticosterone cytotoxicity. At least two types of receptors for corticosterone have been recognized in the rat brain, type I (corticosterone preferring receptor, CR) and type II (glucocorticoid receptor, GR). In the present study the possible changes in GR immunoreactivity (IR) in various tel- and diencephalic regions of the aged rat have been investigated using immunocytochemistry coupled with computer-assisted image analysis. Male Sprague-Dawley rats of 3, 12 and 24 months of age were used (n = 5/group). A selective decrease of GR-IR was observed in the CA1 hippocampal field and central amygdaloid nucleus of the 24-month-old with respect to both 3- and 12-month-old rats. While in the former region GR-IR decrease was paralleled by a decrease of IR field area, no age-related decrease of GR-IR profile number was detected in central amygdaloid nucleus. A significant decrease of GR-IR and IR field area was also observed in the dentate gyrus of 24- vs 12-month-old rats but not vs 3-month-old rats. The analysis of adjacent sections stained with Cresyl violet showed a pattern of age-related changes (decrease of neuronal profiles in CA1 field pyramidal layer and dentate gyrus granular layer, and no change in the central amygdaloid nucleus of aged rats) which paralleled the observed changes in GR-IR in the same areas. This study provides evidence that GR are selectively decreased in the hippocampal formation and in the central amygdaloid nucleus of the aged rat.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

PubMed1986

Differential effect of chemical lesion and electrocoagulation of the central amygdaloid nucleus on active avoidance responses.

The effect of lesions of the central amygdaloid nucleus on the acquisition of two way active avoidance responses was studied in Wistar male rats. Lesions were carried out by electrocoagulation or by local application of ibotenic acid, a neurotoxin that destroys neuronal cells without damaging fibres passing through the lesioned area. The results showed that both types of lesion lead to a deficit of active avoidance responses, but the impairment with respect to control group was significant only when the neurotoxin was applied. These results suggest that at least the neurons of the central amygdaloid nucleus could play some role for the organization of active avoidance behaviour.

Amygdala↗

PubMed1998

Synaptic responsiveness of interneurons of the cat lateral amygdaloid nucleus.

Previous work in our laboratory has revealed that the excitability of lateral amygdaloid projection neurons is tightly regulated by GABA-mediated inhibitory postsynaptic potentials and intrinsic conductances that can be activated by synaptic inputs. Here, we studied the synaptic responsiveness of lateral amygdaloid interneurons recorded intracellularly in vivo, in the cat, to investigate their role in regulating the activity of projection cells. Interneurons were identified morphologically by their aspiny dendritic trees and physiologically by their ability to generate high frequency, non-adapting spike trains in response to depolarizing current pulses. Cortical shocks of increasing intensity generated opposite response profiles in interneurons and projection cells, with interneurons becoming progressively more excited and projection cells more inhibited. These cortically-evoked response profiles paralleled the activity of interneurons and projection cells in relation to spontaneous electroencephalographic events of differing amplitudes. Only at the lowest intensities were predominantly excitatory responses elicited in both cell types. As a result, only a narrow range of low stimulus intensities could trigger spikes in projection cells. In both cell types, the initial cortically-evoked excitatory postsynaptic potential was followed by a hyperpolarization, which was of markedly lower amplitude and duration in interneurons. In interneurons, the hyperpolarization reversed at approximately -72 mV with potassium acetate pipettes and approximately -55 mV with potassium chloride pipettes, suggesting that this inhibitory postsynaptic potential is primarily mediated by a chloride conductance. In light of previous findings indicating that inhibition in the lateral amygdaloid nucleus arises mostly from local inhibitory neurons, these results suggest that interneurons are synaptically coupled via GABAA receptors. Moreover, the opposite response profiles of interneurons and projection cells to cortical shocks indicate that interneurons play a critical role in regulating the activity of projection cells. The cellular interactions evidenced in the present study suggest that the lateral amygdaloid nucleus is endowed with an inhibitory gating mechanism that regulates information flow through the amygdala.

Amygdala↗

PubMed2006

The effect of 5-HT(2a/2c) receptor agonist microinjected into central amygdaloid nucleus and median preoptic area on maternal aggressive behavior in rats.

OBJECTIVE: Much evidence supports the hypothesis that 5-hydroxytryptamine (5-HT) activation is related to the inhibition of aggression. We examined potentially pro- and anti-aggressive effects of the 5-HT(2A/2C) receptor agonist on specific brain sites. METHOD: Female Wistar rats on the 7th day postpartum were microinjected with the selective 5-HT(2A/2C) receptor agonist, alpha-methyl-5-hydroxytryptamine maleate (0.2 to 1.0 microg/0.2 microl) into the central amygdaloid nucleus and median preoptic nucleus. For each brain area studied, the frequency of the behaviors: locomotion, social investigation, lateral threat, attacks (frontal and lateral), and biting the intruder were compared among the various treatments by an Analysis of Variance, followed when appropriate, by Tukey's test. RESULTS: Microinjection of the selective 5-HT(2A/2C) receptor agonist, a-methyl-5-hydroxytryptamine maleate into central amygdaloid nucleus increased maternal aggression in the absence of concurrent changes in non-aggressive behavior. By contrast, microinjection of the selective 5-HT(2A/2C) receptor agonist at several dilutions into the median preoptic nucleus did not alter aggressive behavior. CONCLUSIONS: The current and earlier data with pro- and anti-aggressive effects of the 5-HT(2a/2c) receptor agonist, when microinjected into the median preoptic nucleus relative to the central amygdaloid nucleus, medial septum and periaqueductal grey area in female rats point to functionally separate serotonin receptor populations in the amygdaloid-septal-hypothalamic and periaqueductal gray matter areas controlling aggressive behavior. It is possible that amygdaloid 5-HT(2a/2c) receptors may increase aggressive behavior in lactating females as a result of changes in fear.

Aggression↗

PubMed1989

The organization of dorsal medullary projections to the central amygdaloid nucleus and parabrachial nuclei in the rabbit.

The amygdaloid central nucleus and the pontine parabrachial nucleus receive direct, ascending projections from autonomic regulatory nuclei of the dorsal medulla and are recognized as important components of a forebrain system which contributes to autonomic regulation. The present study was designed to provide more detailed information on the anatomical organization of this ascending system in the rabbit by determining (a) the extent to which separate populations of neurons within the solitary complex project to the central nucleus and parabrachial nucleus, (b) the topographical distribution of the projections of the solitary complex within the amygdaloid central nucleus and parabrachial nucleus and (c) the extent to which projections from the solitary complex to the parabrachial nucleus terminate in the region of origin of projections from the parabrachial nucleus to the amygdaloid central nucleus. A fluorescent dye, double retrograde-labeling technique demonstrated that separate populations of neurons in the solitary complex projected to the amygdaloid central nucleus and parabrachial nucleus. Neurons of both populations were more heavily concentrated within the caudal two thirds of nucleus of the solitary tract and were most numerous within the commissural, medial and dorsomedial subnuclei. Labeled neurons were also located within the dorsal motor nucleus of the vagus nerve. Autoradiographic experiments demonstrated that injections of amino acids into the solitary complex resulted in terminal labeling in the central nucleus. This labeling extended rostrally into the adjacent sublenticular substantia innominata and lateral component of the bed nucleus of the stria terminalis. Label was also observed within the lateral, medial, and Kolliker-Fuse regions of the parabrachial nucleus. A particularly dense field was observed overlying cells located within the ventrolateral region of the lateral parabrachial nucleus. This region contained the majority of labeled neurons within the parabrachial nucleus following fluorescent dye injections into the central nucleus. Furthermore, injections of amino acids into this region resulted in terminal labeling within the central nucleus, with a particularly dense area observed within the medial aspect of the nucleus. The results demonstrate that separate populations of neurons within the solitary complex of the rabbit project to the central amygdaloid and parabrachial nuclei and that the majority of these are located within the caudal two-thirds of the complex.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗

PubMed1984

Central amygdaloid nucleus lesion attenuates exaggerated hemodynamic responses to noise stress in the spontaneously hypertensive rat.

The regional hemodynamic basis of the cardiovascular response to acute noise stress in spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats and the role of the central amygdaloid nucleus in mediating this response was investigated. Using the pulsed Doppler flow probe technique it was determined that in response to noise, SHR exhibit a significantly greater percent increase in renal and mesenteric vascular resistance than WKY. Vascular responses in the hindquarter were similar in both groups. Bilateral lesion of the central amygdaloid nucleus or its output pathways to the brainstem decreased the cardiovascular response to noise in both SHR and WKY, with SHR and WKY lesion rats responding similarly. The central amygdaloid nucleus appears to participate in the cardiovascular response to acute noise stress in SHR and WKY. Although other structures in the limbic system network may contribute to integration of responses that involve the amygdala the present data suggest that this structure may play a central role in mediating the exaggerated cardiovascular responsiveness of SHR to environmental stress.

Amygdala↗

PubMed1992

A species-specific population of tyrosine hydroxylase-immunoreactive neurons in the medial amygdaloid nucleus of the Syrian hamster.

The medial amygdaloid nucleus (Me) is part of a neural pathway that regulates sexual behavior in the male Syrian hamster. To characterize the neurochemical content of neurons in this nucleus, brains from colchicine-treated adult male and female hamsters were immunocytochemically labeled using antibodies that recognize the catecholamine-synthesizing enzymes, tyrosine hydroxylase (TH), dopamine-beta-hydroxylase (DBH) and phenylethanolamine-N-methyltransferase (PNMT), as well as dopamine. A large population of TH-immunoreactive (TH-IR) neurons was observed throughout Me of male and female hamsters, primarily concentrated in the midrostral and caudal portions of the nucleus. The somata were generally small to medium in size and bipolar. Brains from animals that did not receive colchicine contained a limited number of TH-IR neurons in Me as reported previously. The DBH and PNMT antisera did not label any cells in Me of colchicine-treated animals, and the dopamine antiserum labeled neurons in the same location as the caudal group of TH-IR cells. Therefore, these caudal TH-IR neurons are interpreted to be dopaminergic. The rostral group of TH-IR neurons, on the other hand, may be producing only the immediate precursor of dopamine, L-3,4-dihydroxyphenylalanine (L-DOPA). The TH-synthesizing neurons in Me of the Syrian hamster appear to be a species-specific group of cells located outside of the previously described catecholaminergic cell groups.

Amygdala↗

PubMed1988

Presence of a substance P-like immunoreactive neurone system from the parabrachial area to the central amygdaloid nucleus of the rat with reference to coexistence with calcitonin gene-related peptide.

An ascending neurone system containing substance P-like immunoreactivity (SPI) from the lateral parabrachial nucleus (PBL) to the central amygdaloid nucleus (AC) was detected. Destruction of the external subdivision of the PBL resulted in a marked ipsilateral reduction of SPI fibres in the AC, which suggests that SPI neurones project mainly ipsilaterally to the AC. This was supported by the findings that injection of biotin-wheatgerm agglutinin into the AC labelled many neurones in the ipsilateral external subdivision of the PBL. Simultaneous staining with antiserum showed that some of these neurones contain SP. Immunohistochemical double-staining revealed that almost all of the SPI neurones in the external subdivision of the PBL contained calcitonin gene-related peptide.

Amygdala↗

PubMed1992

Fos and jun in rat central amygdaloid nucleus and paraventricular nucleus after stress.

The present paper describes the effect of capsaicin-induced stressful stimulus on the expression of immediate early genes (IEGs) c-fos, c-jun, junB and junD in the hypothalamic paraventricular nucleus (PVN) and the central amygdaloid nucleus (ACe) using in situ hybridization. Stress caused an intense expression of c-fos, c-jun and junB especially in the PVN and ACe and also a clear induction of junD was observed in the PVN. This suggests that the PVN and the ACe are two major targets of stress in the brain. The intense expression of the IEGs in the ACe and PVN suggests that stress may affect neurotransmitter gene expression through Fos and Jun proteins in both these nuclei.

Amygdala↗

PubMed1987

Open field activity and passive avoidance responses in rats after lesion of the central amygdaloid nucleus by electrocoagulation and ibotenic acid.

The effect of two types of bilateral lesion of the central amygdaloid nucleus on open field activity and on the acquisition of a passive avoidance conditioning in a run way was studied in male Wistar rats. The animals were divided into three groups: sham-operated, a group with lesions caused by electrocoagulation, and a third group lesioned by local application of ibotenic acid. Ibotenic acid is a neurotoxin which damages the neurons but spares the passing fibres. The results indicate that lesion by electrocoagulation leads to a significant increase in the number of rearing responses in the open field. Moreover, lesion by electrocoagulation, but not by ibotenic acid, leads to a deficit in the acquisition of passive avoidance conditioning. This latter result suggests that the deficit is caused by lesion of the fibres crossing the central amygdaloid nucleus and not by the intrinsic elements of the nucleus.

Amygdala↗

PubMed1991

Inhibition of jaw-opening reflex by stimulation of the central amygdaloid nucleus in the cat.

The effect of stimulation of the amygdaloid complex on the jaw-opening reflex (JOR) was studied in the cat anesthetized with pentobarbital sodium. The conditioning stimulation of the central amygdaloid nucleus (ACE), but not the other amygdaloid nuclei, markedly inhibited the JOR induced by the tooth pulp stimulation. Ipsilateral ACE conditioning stimulation with 300 microA produced inhibition which lasted approximately 500 ms from the cessation of the stimulation. Additionally, the microinjection of monosodium glutamate into ACE elicited inhibition of the JOR that lasted about 10 min. These findings suggest that the excitation of the cell bodies in ACE exerts inhibitory action on the trigeminal nociceptive reflex.

Amygdala↗

PubMed1988

Plasticity of intra-amygdaloid connections following the denervation of fibers from accessory olfactory bulb to medial amygdaloid nucleus in adult rat: immunohistochemical study of anterogradely transported lectin (Phaseolus vulgaris leucoagglutinin).

The rearrangement of the terminations of intra-amygdaloid fibers was examined in the medial amygdaloid nucleus (MAN) following denervation of the fibers from the accessory olfactory bulb (AOB) of adult rat using immunohistochemistry of anterogradely transported lectin (Phaseolus vulgaris leucoagglutinin, PHA-L). The AOB was removed unilaterally by suction at two months before the PHA-L injection. The PHA-L was injected bilaterally into the posteromedial region of the amygdala (posteromedial amygdaloid nucleus and amygdala-hippocampal transitional area). After the tissue was processed by the routine immunohistochemical method, the immunologically labeled axons and axon terminals in the MAN were observed with the light microscope. On the control side, labeled axons were observed in the cellular part of the MAN, but they were not found in the molecular layer in which the fibers from the accessory olfactory bulb terminate. On the side of the AOB removal, the labeled axons were found not only in the cellular part but also in the molecular layer. Electron microscopic observations showed that the labeled axon terminals made synaptic contacts in the molecular layer. These results indicate that terminals of intra-amygdaloid fibers expand from the cellular part to the molecular layer in the MAN and make synaptic contacts in this layer following the denervation of the AOB fibers.

Amygdala↗