Lateral inhibition and granule cell synchrony in the rat hippocampal dentate gyrus

作者: RS Sloviter , JL Brisman

DOI: 10.1523/JNEUROSCI.15-01-00811.1995

关键词: PopulationHippocampal formationLateral inhibitionBicucullinePerforant pathGranule (cell biology)NeuroscienceGranule cellDentate gyrusChemistry

摘要: Studies of patients with temporal lobe epilepsy and experimental models this disorder suggest that the hippocampal dentate gyrus may be a common site seizure onset propagation. However, nature “network defect” could give rise to spontaneous, intermittent, synchronous population discharges is poorly understood. We have hypothesized large expanses granule cell layer an underlying tendency discharge synchronously in response afferent excitation, but do not so normally because vulnerable hilar neurons establish lateral inhibition thereby prevent focal from spreading surrounding segments. To address hypothesis, we (1) identified functionally independent segments layer; (2) determined whether one segment evoke segments; and, (3) if disinhibition induces synchronously. Simultaneous extracellular recordings were made two locations along longitudinal or transverse axes using saline- bicuculline- filled electrodes glued together. Leakage 10 mM bicuculline electrode tip produced no detectable spontaneous activity. single perforant path stimuli evoked multiple spikes at simultaneous normal responses nearby saline electrode. The did propagate to, detected by, adjacent electrode, indicating functional separation between neighboring subgroups cells. Paired-pulse stimulation revealed only restricted layer, strongly inhibited This often lasted longer than 150 msec. Finally, evaluated activity sites within both before after was induced by high frequency stimulus trains injection. Following sec, 20 Hz train, 2 virtually identical synchronized epileptiform separated sites. Similarly, intrahippocampal intravenous injection throughout layer. These results indicate “surround” operant physiological mechanism disinhibited network highly are kept GABA-mediated inhibition.

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