Cellular mechanisms of cobalt-induced hippocampal epileptiform discharges.
OBJECTIVE
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.


CONCLUSIONS
Mechanisms involving activity-dependent facilitation of gap junctional communication may play a major role in cobalt-induced epileptiform discharges.
He
Jiwei
J
Toronto Western Research Institute, University Health Network, Toronto, ON, Canada.
Hsiang
Hwa-Lin
HL
Wu
Chiping
C
Mylvagnanam
Shanthini
S
Carlen
Peter L
PL
Zhang
Liang
L
D000818:Animals; D000927:Anticonvulsants / Q000627:therapeutic use; D016587:Antimutagenic Agents / Q000009:adverse effects*; D015220:Calcium Channels / Q000187:drug effects; D003035:Cobalt / Q000009:adverse effects*; D004569:Electroencephalography; D004827:Epilepsy / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology*; D017629:Gap Junctions / Q000187:drug effects; D006624:Hippocampus / Q000473:pathology* / Q000503:physiopathology*; D051379:Mice; D008810:Mice, Inbred C57BL; D017966:Pyramidal Cells / Q000187:drug effects / Q000473:pathology; D018079:Receptors, GABA / Q000187:drug effects
D000927:Anticonvulsants; D016587:Antimutagenic Agents; D015220:Calcium Channels; D018079:Receptors, GABA; D003035:Cobalt; C018021:cobaltous chloride