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The Effect of Calcium Channel Antagonists on Spontaneous and Evoked Epileptiform Activity in the Rat Neocortex In Vitro
Author(s) -
Boulton Caroline L.,
O'Shaughnessy Celestine T.
Publication year - 1991
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.1991.tb00035.x
Subject(s) - verapamil , chemistry , neocortex , calcium channel , p type calcium channel , voltage dependent calcium channel , t type calcium channel , calcium , bursting , nifedipine , stimulation , agonist , neuroscience , medicine , endocrinology , receptor , psychology , biology , biochemistry , organic chemistry
Calcium influx through voltage‐activated calcium channels may play a crucial role in the propagation and maintenance of seizure activity. We have examined the contribution of various types of calcium currents to epileptogenesis by studying the effects of various calcium channel blockers on epileptiform activity. N ‐methyl‐ d ‐aspartate receptor‐mediated epileptiform activity was induced by removal of magnesium ions superfusing the cortex, or by low‐frequency stimulation of the underlying white matter. CoCl 2 , CdCl 2 and ω‐conotoxin, acting at the N‐ and L‐type calcium channels, significantly reduced epileptiform activity. L‐channel antagonists nifedipine and verapamil, and the agonist BAY K 8644, increased spontaneous bursting in cortical wedges, but had no effect upon evoked activity. The T‐channel blocker NiCI 2 had variable effects on epileptiform activity, whereas phenytoin consistently reduced such activity. These results suggest that calcium influx underlying epileptiform activity in the rat neocortex may occur at least partially via the activation of the N‐type calcium channel. However, contributions from other calcium channel types cannot be excluded.