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Cellular mechanisms of cobalt‐induced hippocampal epileptiform discharges
Author(s) -
He Jiwei,
Hsiang HwaLin,
Wu Chiping,
Mylvagnanam Shanthini,
Carlen Peter L.,
Zhang Liang
Publication year - 2009
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1167.2008.01767.x
Subject(s) - hippocampal formation , ictal , neuroscience , extracellular , cobalt , excitatory postsynaptic potential , chemistry , gap junction , epilepsy , hippocampus , population , electrophysiology , medicine , psychology , intracellular , biochemistry , inhibitory postsynaptic potential , inorganic chemistry , environmental health
Summary Purpose: To explore the cellular mechanisms of cobalt‐induced epileptiform discharges in mouse hippocampal slices. Methods: Hippocampal slices were prepared from adult mice and briefly exposed to a CoCl 2 ‐containing external solution. Population and single cell activities were examined via extracellular and whole‐cell patch recordings. Results: Brief cobalt exposure induced spontaneous, ictal‐like discharges originating from the CA3 area. These discharges were suppressed by anticonvulsants, gap junction blockers, or by raising extracellular Ca 2+ , but their generation was not associated with overall hyperexcitability or impairment in GABAergic inhibition in the CA3 circuit. Electroencephalographic ictal discharges of similar waveforms were observed in behaving rats following intrahippocampal cobalt infusion. Discussion: Mechanisms involving activity‐dependent facilitation of gap junctional communication may play a major role in cobalt‐induced epileptiform discharges.