Cellular mechanisms of cobalt-induced hippocampal epileptiform discharges

Epilepsia. 2009 Jan;50(1):99-115. doi: 10.1111/j.1528-1167.2008.01767.x. Epub 2008 Aug 25.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anticonvulsants / therapeutic use
  • Antimutagenic Agents / adverse effects*
  • Calcium Channels / drug effects
  • Cobalt / adverse effects*
  • Electroencephalography
  • Epilepsy / drug therapy
  • Epilepsy / etiology*
  • Epilepsy / physiopathology*
  • Gap Junctions / drug effects
  • Hippocampus / pathology*
  • Hippocampus / physiopathology*
  • Mice
  • Mice, Inbred C57BL
  • Pyramidal Cells / drug effects
  • Pyramidal Cells / pathology
  • Receptors, GABA / drug effects

Substances

  • Anticonvulsants
  • Antimutagenic Agents
  • Calcium Channels
  • Receptors, GABA
  • Cobalt
  • cobaltous chloride