NDLI: Initial loss but later excess of GABAergic synapses with dentate granule cells in a rat model of temporal lobe epilepsy.

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Initial loss but later excess of GABAergic synapses with dentate granule cells in a rat model of temporal lobe epilepsy.

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Initial loss but later excess of GABAergic synapses with dentate granule cells in a rat model of temporal lobe epilepsy.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Thind, Khushdev K. Yamawaki, Ruth Phanwar, Ibanri Zhang, Guofeng Wen, Xiling Buckmaster, Paul S.
Description	Country affiliation: United States Author Affiliation: Thind KK ( Department of Comparative Medicine, Stanford University, California 94305, USA.)
Abstract	Many patients with temporal lobe epilepsy display neuron loss in the dentate gyrus. One potential epileptogenic mechanism is loss of GABAergic interneurons and inhibitory synapses with granule cells. Stereological techniques were used to estimate numbers of gephyrin-positive punctae in the dentate gyrus, which were reduced short-term (5 days after pilocarpine-induced status epilepticus) but later rebounded beyond controls in epileptic rats. Stereological techniques were used to estimate numbers of synapses in electron micrographs of serial sections processed for postembedding GABA-immunoreactivity. Adjacent sections were used to estimate numbers of granule cells and glutamic acid decarboxylase-positive neurons per dentate gyrus. GABAergic neurons were reduced to 70% of control levels short-term, where they remained in epileptic rats. Integrating synapse and cell counts yielded average numbers of GABAergic synapses per granule cell, which decreased short-term and rebounded in epileptic animals beyond control levels. Axo-shaft and axo-spinous GABAergic synapse numbers in the outer molecular layer changed most. These findings suggest interneuron loss initially reduces numbers of GABAergic synapses with granule cells, but later, synaptogenesis by surviving interneurons overshoots control levels. In contrast, the average number of excitatory synapses per granule cell decreased short-term but recovered only toward control levels, although in epileptic rats excitatory synapses in the inner molecular layer were larger than in controls. These findings reveal a relative excess of GABAergic synapses and suggest that reports of reduced functional inhibitory synaptic input to granule cells in epilepsy might be attributable not to fewer but instead to abundant but dysfunctional GABAergic synapses.
File Format	HTM / HTML
ISSN	00219967
e-ISSN	10969861
DOI	10.1002/cne.22235
Journal	Journal of Comparative Neurology
Issue Number	5
Volume Number	518
Language	English
Publisher	Wiley
Publisher Date	2010-03-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Neurology Dentate Gyrus Pathology Epilepsy, Temporal Lobe Neurons Synapses Gamma-aminobutyric Acid Metabolism Animals Cell Count Convulsants Dendritic Spines Physiopathology Disease Models, Animal Glutamate Decarboxylase Interneurons Microscopy, Immunoelectron Nerve Degeneration Etiology Neural Inhibition Physiology Neurogenesis Neuronal Plasticity Pilocarpine Recovery Of Function Status Epilepticus Chemically Induced Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Neuroscience

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