The voltage-sensitive Ca2+ channel (VSCC) antagonists ω-Aga-IVA and ω-CTX-MVIIC inhibit spontaneous epileptiform dischares in the rat cortical wedge

Abstract The ability of VSCC antagonists to modulate excitatory amino acid (EAA) release was evaluated by measuring N -methyl- d -aspartate (NMDA) receptor-dependent spontaneous epileptiform discharges in rat cortical wedges. The N-type channel blocker ω-CTX-GVIA (300 nM) was ineffective. The P-type channel blocker ω-Aga-IVA at 300 nM reduced the frequency of discharges by 63%, while 300 nM ω-CTX-MVIIC reduced the frequency by 35%. These results coupled with the absence of NMDA antagonism by ω-Aga-IVA or ω-CTX-MVIIC in the cortical wedge suggest that the VSCCs blocked by these toxins are primarily responsible for mediating impulse dependent EAA release in the rat neocortex.