240 research outputs found
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DIFFERENCES IN THE HIPPOCAMPAL GABAERGIC SYSTEM BETWEEN SEIZURE-SENSITIVE AND SEIZURE-RESISTANT GERBILS
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Increased numbers of GABAergic neurons occur in the inferior colliculus of an audiogenic model of genetic epilepsy.
The numbers of GABAergic neurons as determined by GAD immunocytochemistry and total neurons as determined from Nissl preparations were counted and classified at the light microscopic level in the inferior colliculus (IC) of the genetically epilepsy-prone rat (GEPR) and the non-epileptic Sprague-Dawley (SD) strain of rat. GAD-positive neurons are abundant in the IC in all 3 subdivisions. Several sizes of multipolar neurons as well as medium-sized bipolar or fusiform neurons are GAD-positive. GAD-positive punctate structures that were interpreted to be axon terminals and transversely-sectioned dendrites and preterminal axons are abundant in the IC of both the GEPR and SD. A dramatic increase in the number of GAD-positive neurons occurs in the GEPR as compared to the SD. This increase is most evident in the middle of the rostrocaudal extent of the IC. Although the increase is statistically significant in all subdivisions of the IC, it is most pronounced in the central nucleus, especially the ventral lateral portion. Within the central nucleus, the increase in the number of GAD-positive neurons is due to a selective increase in the small (200%) and medium (90%) cell body size populations (10-15 micron and 15-25 micron in diameter, respectively). Concomitant with this increase in the number of GAD-positive neurons, an increase in total numbers of neurons occurs as determined from Nissl preparations. A 100% increase in the number of small neurons and a 30% increase in the number of medium-sized neurons occur in the GEPR as compared to the SD rat. The proportion of GAD-positive neurons to total neurons is also increased in the GEPR. Approximately 25% of the neurons in the IC in SD rat are GAD-positive, while about 35% of the neurons in the GEPR are GAD-positive. These data demonstrate an anatomical difference in the IC of the GEPR as compared to the SD which appears to be preferential for the GABAergic system
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A regional increase in the number of hippocampal GABAergic neurons and terminals in the seizure-sensitive gerbil.
Inhibitory gamma-aminobutyric acidergic (GABAergic) neurons were identified in the dentate gyrus of seizure-sensitive (SS) and seizure-resistant (SR) gerbils by immunocytochemical localization of glutamic acid decarboxylase (GAD), the synthesizing enzyme for GABA. Increases in both the number of GAD+ somata and terminals were found in the dentate gyrus of the SS brains compared to the SR. The magnitude of the increase was positively correlated with the recorded seizure intensity. The increased number of GABAergic neurons in the dentate gyrus of SS gerbils could result in disinhibition of the granule cells, thereby allowing propagation of epileptiform activity through the hippocampus
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GABAERGIC NEURONAL SOMATA DECREASE AT SITES OF FOCAL EPILEPSY IN MONKEY NEOCORTEX
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A decrease in the number of GABAergic somata is associated with the preferential loss of GABAergic terminals at epileptic foci.
Previous studies have indicated that a loss of GABAergic terminals occurs at epileptic foci. The present study was undertaken to investigate if this loss is associated with a loss of GABAergic neuronal somata. Seven juvenile monkeys (M. mulatta) received alumina gel injections to the pre-central gyrus of the left cerebral hemisphere to produce epileptic foci. Four of these monkeys were chosen for further quantitative study. One was sacrificed prior to seizure onset ('pre-seizure'), one had seizures for 3 days ('acute'), and two had a seizure record of one month ('chronic'). Sections of tissue from the epileptic cortex and from the contralateral, non-epileptic cortex were processed for glutamate decarboxylase (GAD) immunocytochemistry at the light microscopic level. Quantitative analysis revealed that a loss of GAD-positive neuronal somata ranging from 24 to 52% occurred at epileptic foci for all monkeys. This decrease was significant (P less than 0.01) for the two chronic monkeys. There was also a slight decrease in GAD-positive neurons 1 cm distal to the focus ('parafocus') in the chronic monkeys, but not in the acute or pre-seizure animals. In addition, small GAD-positive somata (50-150 micron2) were more severely decreased in number at epileptic foci than larger ones (200-250 micron2). As an experimental control, an additional monkey was given a surgical lesion in area 4 of one cerebral hemisphere. It did not display seizure activity prior to sacrifice and did not show a loss of GAD-positive neurons proximal to the control lesions. The results of this study indicate that a loss of GABAergic neuronal somata is associated with a loss of GABAergic terminals at epileptic foci, and that this loss may be more specific for the small GABAergic neurons
A description of the GABAergic neurons and axon terminals in the motor nuclei of the cat thalamus.
The GABA neurons and their processes in the cat motor thalamic nuclei were identified and studied with glutamic acid decarboxylase (GAD) immunocytochemistry at both the light and electron microscopic levels. The three nuclei that comprise the motor thalamus, ventral anterior (VA), ventral medial (VM), and ventral lateral (VL), each displayed a characteristic distribution pattern of GAD-positive structures that was consistent with their afferent and intrinsic neuronal organization. All three thalamic nuclei displayed a population of small, GAD-positive cells the dendrites of which contained synaptic vesicles and participated in complex synaptic arrays such as serial synapses, triads, and glomeruli. Based on their ultrastructural features, these GAD-containing cells were identified as local circuit neurons. In contrast, the larger, GAD-negative cells were presumed to be the thalamocortical projection neurons. The axons of GAD-positive local circuit neurons could not be identified in these preparations. The number of GAD-positive dendrites in the neuropil was different for the three thalamic nuclei. In the VA and VM, the GAD-positive dendrites were numerous and formed symmetric synapses with dendrites of GAD-negative cells, mainly in association with corticothalamic boutons. Within VL, the GAD-containing dendrites were more numerous than in VA and VM and formed synapses at influential locations on presumed thalamocortical projection neurons, such as bases of primary dendrites, and bifurcation sites of primary and secondary dendrites. The VA and anterolateral VM nuclei that receive inhibitory GABAergic afferents from the entopeduncular nucleus and substantia nigra contained the highest concentration of large GAD-positive axon terminals. These boutons contained pleomorphic vesicles and numerous mitochondria and formed symmetric synapses and multiple puncta adherentes with dendrites and somata of presumed thalamocortical projection neurons. The size, ultrastructural features, and distribution of these GAD-positive boutons were similar to those features described for basal ganglia terminals in the motor thalamus of the cat. In addition, similar large-size GAD-positive boutons were observed in the medial VM, which receives basal ganglia afferents exclusively from the substantia nigra. The concentration of these terminals in medial VM along the dendrites of thalamocortical projection neurons was much less than that in VA and anterolateral VM. The VL nucleus which lacks basal ganglia input did not contain any large GAD-positive boutons.(ABSTRACT TRUNCATED AT 400 WORDS
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THE HIPPOCAMPAL COMMISSURAL PATHWAY CONTAINS A GABAERGIC INHIBITORY COMPONENT
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