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At least 109 records · Page 6Linked to original sources

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↗

PubMed1999

Effects of conditioning stimulation of the central amygdaloid nucleus on tooth pulp-driven neurons in the cat somatosensory cortex (SI).

To study the limbic control of nociception, we examined the effect of conditioning stimulation of the central amygdaloid nucleus (ACE) on tooth pulp-driven (TPD) neurons in the first somatosensory cortex (SI). Cats were anesthetized with N(2)O-O(2) (2:1) and 0.5% halothane, and immobilized with tubocurarine chloride. The tooth pulp test stimulus was applied by a single rectangular pulse (0.5 ms in duration and 3-5 times the threshold intensity for the jaw-opening reflex). Conditioning stimuli to the ACE consisted of trains of 33 pulses (300 microA) delivered at 330 Hz at intervals of 8-10 s. In 35 out of 61 of the slow (S)-type TPD neurons with latencies of more than 20 ms, conditioning stimulation in the ACE, especially in the medial division, markedly reduced the firing response to the pulpal stimulation. The inhibition of the firing rate in the S-type neurons was 74% of the control. In these S-type neurons, the neurons that were inhibited had significantly longer latencies compared to the non-inhibited neurons (45.0 +/- 17.6 ms, n = 32 vs. 34.8 +/- 10.5 ms, n = 26). In contrast, the ACE conditioning stimulation affected only one out of 18 fast-type TPD neurons with latencies of less than 20 ms. In addition, ACE stimulation had no effect on the spontaneous discharges of either S-type or F-type neurons. The ACE inhibitory effect on S-type neurons was not diminished by naloxone administration (1 mg/kg, I.V. ), while the blockade of histamine H(1)-receptor by diphenhydramine hydrochloride (0.5 mg/kg, I.V.) partially reversed the inhibitory effect. These results suggest that the ACE inhibits ascending nociceptive information to the SI and that this inhibition is mediated in part by histamine (H(1)) receptors. It seems likely that the antinociceptive effect is a neurophysiological basis for stress-induced analgesia (SIA).

Amygdala↗

PubMed1995

Association between intermale social aggression and cellular density within the central amygdaloid nucleus in rats with lithium/pilocarpine-induced seizures.

Aggressive behaviors (numbers of bites/hour) within groups (ns = 8) of normal rats and rats in which seizures had been induced by a single systemic injection of lithium/pilocarpine were observed for 11 successive, 1-hr, periods. Mean numbers of neurons and glial cells were counted for 10 different nuclei of the amygdala for 16 different brains (8 control; 8 seizure). Although there was no significant difference found between rats with chronically induced seizures and controls for the numbers of neurons per area within the central medial amygdaloid nucleus, the neuronal density was correlated significantly (.92) with mean numbers of bites per hour for the chronically epileptic group only. The hypothesis that seizure-induced damage within proximal amygdaloid nuclei disinhibits the central nucleus and encourages aggression was supported.

Aggression↗

PubMed1998

Electrical self-stimulation in the central amygdaloid nucleus after ibotenic acid lesion of the lateral hypothalamus.

This experiment was carried out in order to investigate the involvement of lateral hypothalamus (LH) in electrical self-stimulation of the central amygdaloid nucleus (CeA). Adult male Sprague-Dawley rats were bilaterally implanted with a guide cannula situated above each LH and with two electrodes in the CeA. Self-stimulation was subsequently obtained separately from both right and left electrodes. The LH was then lesioned unilaterally by ibotenic acid (IBO) injection. Eight days later, the effect of this unilateral lesion on self-stimulation of the ipsilateral and contralateral CeA was tested. Then the neurons of the remaining non-lesioned LH side were lesioned with IBO and self-stimulation was tested 15 days after the second lesion. Both unilateral as well as bilateral lesions of LH produced a significant decrease in CeA self-stimulation rates but had no significant effect on the reward effectiveness. The unilateral lesions did not produce any modification of the rate-intensity function in the contralateral CeA. This lesion-induced depression in performance was reversed by treatment with phenobarbital. These results provide clear evidence that the rewarding effects of CeA electrical stimulation do not result from the activation of the LH outputs and that the apparent decrease in CeA self-stimulation may result from the LH lesion-induced increase in the frequency of epileptiform manifestations that occur following amygdaloid stimulation.

Amygdala↗

PubMed1978

Biologically active pituitary hormones in the rat brain amygdaloid nucleus.

While an attempt was being made to identify the source of the growth hormone releasing factor present in cerebral spinal fluid of man, it was discovered that cells of the rat amygdaloid nucleus, grown in tissue culture, produce a material that is immunologically and chromatographically identical to growth hormone found in the pituitary. Immunoperoxidase staining revealed dense accumulation of the peroxidase-antibody to growth hormone complex in amygdala cells. Significant amounts of growth hormone and adrenocorticotropin could be extracted from this limbic structure. Extracts containing immunoequivalent amounts of growth hormone were measured by bioassay in hypophysectomized rats. Stimulation of the growth of epiphyseal cartilage by extracts of the amygdala was comparable to the stimulation by extracts of anterior pituitary glands. The stimulatory effect of amygdala extracts on adrenal and gonadal size and weight and on growth of thyroid follicular epithelium was also comparable to that of pituitary extracts.

Adrenal Glands↗

PubMed1993

Tyrosine hydroxylase mRNA-containing neurons in the medial amygdaloid nucleus and the reticular nucleus of the thalamus in the Syrian hamster.

To confirm previous immunocytochemical findings in colchicine-treated Syrian hamsters, in situ hybridization was used to investigate the distribution of TH mRNA-containing cells in the medial amygdaloid nucleus (Me) and the thalamic reticular nucleus (Rt) of untreated hamsters. TH mRNA-producing neurons were observed in anterior and posterior Me and throughout Rt, similar to the distribution of TH-immunostained cells in these areas of animals receiving colchicine. These data confirm that TH is normally produced in amygdaloid and thalamic cell groups which lie outside the classical catecholamine systems.

Amygdala↗

PubMed1983

Tolerance to amphetamine-induced inhibition of neuronal activity in the central amygdaloid nucleus.

Rats were pretreated twice daily for 5 consecutive days with saline or 2.5 mg/kg d-amphetamine. Approximately 12 hr after the last injection, neuronal activity was recorded bilaterally from the central amygdaloid nucleus (CAN) and the animals were challenged every 2 min with 0.2 mg/kg d-amphetamine or with increasing incremental doses of apomorphine. In saline controls, all CAN neurons were inhibited by the 5th amphetamine injection and two-thirds were suppressed by 0.64 mg/kg apomorphine. In amphetamine-pretreated animals, on the other hand, the majority of CAN neurons failed to respond even by the 10th amphetamine injection and less than one-third were inhibited by apomorphine even at a dose of 2.56 mg/kg. These results indicate that tolerance develops to the inhibitory effects of d-amphetamine in the CAN and that this effect is mediated, at least in part, by a decrease in the sensitivity of postsynaptic dopamine receptors.

Amygdala↗

PubMed1998

Bidirectional connections of the medial amygdaloid nucleus in the Syrian hamster brain: simultaneous anterograde and retrograde tract tracing.

In the male Syrian hamster, mating is dependent on chemosensory and hormonal stimuli, and interruption of either input prevents copulation. The medial amygdaloid nucleus (Me) is a key nodal point in the neural circuitry controlling male sexual behavior because it relays both odor and steroid cues. Me is comprised of two major subdivisions, anterior (MeA) and posterior (MeP), which have distinct, although overlapping efferent projections. The present study investigated the afferents and efferents of MeA and MeP by using combined anterograde and retrograde tract tracing. Phaseolus vulgaris-leucoagglutinin and cholera toxin B were injected by iontophoresis through a single glass micropipette and detected by immunohistochemistry. MeA has widespread connections with olfactory structures, whereas MeP is heavily interconnected with steroid-responsive brain regions. The efferent projections of MeA and MeP were similar to those reported previously for the rat and hamster. In particular, MeP projects to the posteromedial subdivision of the bed nucleus of the stria terminalis (BNST) and to the medial preoptic nucleus, whereas MeA projects to adjacent subnuclei in BNST and the preoptic area. MeA and MeP also have distinct patterns of afferent input. Furthermore, the combination of anterograde and retrograde tract tracers shows that MeA and MeP are each bidirectionally connected with each other and with limbic nuclei. These results demonstrate that subnuclei of Me are interconnected with limbic structures in hamster brain. These connections may contribute to chemosensory and hormonal integration to control male sexual behavior.

Amygdala↗

PubMedDate not supplied

The effect of intrahippocampal injections of serotonin on bioelectrical activity of Gyrus cinguli and amygdaloid nucleus in the rabbit.

The effect of injection of serotonin (5-HT), dissolved in 2 mul of bidistilled water, into hippocampus was studied in rabbits with chronically implanted electrodes and cannulas. Bioelectric activity of gyrus cinguli, amygdaloid nucleus, and dorsal hippocampus was recorded. 5-HT (10--20 mug) inhibited the electrical activity of the structures investigated, and this inhibition was accompanied by a suppression of locomotor activity or sleep.

Amygdala↗

PubMed1992

Synaptic contacts between CGRP-immunoreactive terminals and enkephalin-immunoreactive neurons in the central amygdaloid nucleus of the rat.

An immunoelectron microscopic method combined with immunofluorescence double staining was carried out to examine the relationship between calcitonin gene-related peptide (CGRP)-like immunoreactive (LI) axon terminals and enkephalin (ENK)-LI neurons in the central amygdaloid nucleus (Ce) of the rat. The latter method showed that many ENK-LI cell bodies are densely surrounded by CGRP-LI axons in the lateral subdivision of the Ce (CeL). After taking fluorescence micrographs, the immunoperoxidase technique was used to examine the CGRP-LI axonal profiles under an electron microscope. CGRP-LI terminals were frequently found to form axo-somatic synaptic contacts with ENK-LI neurons in the CeL.

Amygdala↗

PubMed1990

The lateral amygdaloid nucleus: sensory interface of the amygdala in fear conditioning.

Previous work has implicated projections from the acoustic thalamus to the amygdala in the classical conditioning of emotional responses to auditory stimuli. The purpose of the present studies was to determine whether the lateral amygdaloid nucleus (AL), which is a major subcortical target of projections from the acoustic thalamus, might be the sensory interface of the amygdala in emotional conditioning. Lesions were placed in AL of rats and the effects on emotional conditioning were examined. Lesions of AL, but not lesions of the striatum above or the cortex adjacent to the AL, interfered with emotional conditioning. Lesions that only partially destroyed AL or lesions placed too ventrally that completely missed AL had no effect. AL lesions did not affect the responses elicited following nonassociative (random) training. AL is thus an essential link in the circuitry through which auditory stimuli are endowed with affective properties and may function as the sensory interface of the amygdala during emotional learning.

Acoustic Stimulation↗

PubMed2004

GABA mediaties the inhibitory effect of lateral amygdaloid nucleus stimulation on the acoustic response of neurons in A I cortex: An in vivo microiontophoretic study.

Experiments were performed on Sprague Dawley rats with multibarrel microelectrode technique. The effects of acoustic response of A I cortex neurons produced by electrical stimulation of lateral amygdaloid nucleus (LA) and the influence of GABA were observed. Experimental results showed that iontophoretic administration of GABA caused a pronounced inhibition of the electrical activity of A-I neurons. Blockade of GABA(A) with bicuculline (BIC) facilitated the acoustic response. The acoustic response of A-I neurons was inhibited when the LA was stimulated. Iontophoretic application of GABA resulted in a similar inhibitory effect as that of LA stimulation. Blockade of GABA(A) with bicuculline reversed the inhibitory effect of LA stimulation on the acoustic response of A-I neurons. In contrast, application of strychnine, a glycine receptor antagonist, could not reverse the inhibitory effect of LA. Baclofen, a GABA(B) agonist, did not affect the acoustic response of the auditory neurons. These results indicate that GABA is the ultimate transmitter which mediates the LA stimulation-induced inhibition of the acoustic response of A-I neurons in rats, possibly via the GABA(A) receptor.

Acoustic Stimulation↗

PubMed1987

Synaptic reorganization in the medial amygdaloid nucleus after lesion of the accessory olfactory bulb of adult rat. I. Quantitative and electron microscopic study of the recovery of synaptic density.

The time course of the appearance of degenerating synapses and the loss and reappearance of intact synapses was investigated in the medial amygdaloid nucleus (MAN) following lesions of the accessory olfactory bulb (AOB). Degenerating synapses were concentrated in the molecular layer of MAN. A quantitative electron microscopic analysis of the molecular layer was performed at 2, 4, 8, 16, 32 and 64 days after the placement of kainic acid injections within AOB. At each survival time, counts of synapses were made from photomicrographic montages. The degenerating synapses were observed at 2 days after lesion. Their density reached a peak at 2 or 4 days after the lesion and decreased thereafter. No degenerating synapses were found at 64 days following the lesion. Shrinkage of the thickness of molecular layer was observed following the AOB lesion. This was most pronounced at 4 or 8 days after the lesion at which time the thickness was 70-75% of the contralateral molecular layer. The shrinkage receded moderately (85% of contralateral layer at 64 days after lesion). The compensated synaptic density of intact synapses was reduced to less than half of the control density at 4 or 8 days after the lesion. Thereafter synaptic density increased gradually and reached more than 80% of control density at 64 days after lesion. The recovery in number of intact synapses following the lesion suggests the possibility of synaptic reorganization by remaining afferent fibers.

Amygdala↗

PubMed1992

Projection from the ventrolateral medullary neurons containing tyrosine hydroxylase to the central amygdaloid nucleus in the rat.

By using a double-labeling produce of retrograde horseradish peroxidase (HRP) tracing and the immunocytochemical localization of tyrosine hydroxylase (TH), the present study ascertained that the axonal fibers of catecholaminergic neurons in the caudal ventrolateral medulla projected to the central amygdaloid nucleus in the rat. The majority of double-labeled cells were observed primarily around the level of the obex. 92% of HRP retrogradely labeled cells contained TH-like immunoreactive (TH-IR), but only 31% of TH-IR cells was labeled with HRP.

Amygdala↗

PubMed1991

Glutamate-immunoreactive neurons of the central amygdaloid nucleus projecting to the subretrofacial nucleus of SHR and WKY rats: a double-labeling study.

Glutamate immunoreactivity was found in 9%, in the case of Wistar Kyoto rats (WKY), and 14%, in the case of spontaneously hypertensive rats (SHR), of neurons located in the medial division of the central amygdaloid nucleus (CeM) projecting ipsilaterally to the subretrofacial nucleus (SRF) in the rostral ventrolateral medulla using a double-labeling technique in combination with glutamate immunocytochemistry. The results indicate that possibly-glutamatergic neurons located in the CeM project to the SRF, in which vasomotor neurons are present, suggesting involvement of the CeM in blood pressure regulation. No significant difference was found between the distribution of labeled CeM neurons in SHR and WKY rats.

Afferent Pathways↗

PubMed1979

Amygdaloid nucleus syndrome and dehumanization syndrome.

Through statistical tests 3 groups of impulsive-aggressive patients were studied: group 1, 100 individuals with temporal dysrhythmia; group 2, 18 individuals with temporal dysrhythmia submitted either to group analytical therapy or to psychoanalysis; group 3, 25 impulsive-aggressive individuals. Moreover the author differentiates between the amygdaloid nucleus and dehumanization syndromes, through psychoanalytical or psychiatric studies, and stresses the importance of the molding periods in relation to social factors (frustration-aggression-injustice). Amygdalotomy of the hippocampus was suggested in special cases.

Aggression↗

PubMed1992

Vasopressin perfusion within the medial amygdaloid nucleus attenuates prostaglandin fever in the urethane-anaesthetized rat.

The antipyretic effect of arginine vasopressin (AVP) introduced into the ventral septal area (VSA) by push-pull perfusion was investigated in the urethane-anaesthetized rat. In addition, experiments were carried out to determine whether AVP could suppress fever when similarly perfused within the medial amygdaloid nucleus (meA). During push-pull perfusion of artificial cerebrospinal fluid within the VSA or meA, PGE1 injected intracerebroventricularly evoked fevers with respective magnitudes of 1.3 +/- 0.2 degrees C and 1.4 +/- 0.3 degrees C above baseline. Perfusion of AVP (6.5 micrograms/ml) within the VSA had significantly reduced the magnitude of PGE1 fever to 0.3 +/- 0.3 degrees C above baseline, while having no significant effect on afebrile colonic temperature. Perfusion of AVP (6.5 micrograms/ml) within the meA had significantly attenuated the magnitude of PGE1 fever to 0.7 +/- 0.2 degrees C above baseline, while having no significant effect on afebrile colonic temperature. These results support further the utility of the urethane-anaesthetized rat model for future investigations of the central control of fever and antipyresis. In addition, these data are consistent with the hypothesis that AVP may act within the meA as an endogenous antipyretic.

Alprostadil↗

PubMed1995

The medial amygdaloid nucleus and medial preoptic area mediate steroidal control of sexual behavior in the male Syrian hamster.

An important goal of studies on steroid receptors in the brain is to understand the functions of specific populations of steroid receptor-containing neurons, particularly in the control of sexual behavior. The present study compared the ability of testosterone implants directed toward the medial amygdaloid nucleus (Me) or the bed nucleus of the stria terminalis (BNST) and medial preoptic area (MPOA) to stimulate mating in castrated males. Twenty adult male hamsters were selected for vigorous sexual behavior, and baseline measures of copulatory behavior during the first 10 min of a 30-min mating behavior test were recorded on two occasions. Twelve weeks after castration, sexual behavior was recorded as before, and each male received a single intracranial implant constructed of 23-gauge tubing packed with crystalline testosterone placed stereotaxically into Me or BNST/MPOA (n = 10 each). Behavior was assessed on two occasions after surgery to determine if implants in Me or BNST/MPOA could stimulate sexual behavior above that observed after castration. In half of the males from each group, testosterone increased the males' interaction with the female, anogenital investigation, mounting, and reduced the latency to the first mount. After completion of behavioral testing, males were perfused and the brains processed for androgen receptor immunocytochemistry to determine the extent of brain regions influenced by the testosterone-filled cannula. In tissues stained rapidly in diaminobenzidine, androgen receptor-containing neurons were visible only in steroid responsive brain regions adjacent to the testosterone implant. This approach revealed that steroid receptors in both the posterior subdivision of Me and in the medial subregions of BNST/MPOA can mediate hormonal control of mating behavior in the male Syrian hamster. Implants placed outside these regions failed to stimulate mating. These results suggest that maintenance of copulatory behavior by gonadal steroids is not transduced by a single brain region, but that steroid effects can be elicited at multiple points along the mating behavior pathway.

Amygdala↗