snx-230 and Epilepsy

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 omega-CTX-GVIA (300 nM) was ineffective. The P-type channel blocker omega-Aga-IVA at 300 nM reduced the frequency of discharges by 63%, while 300 nM omega-CTX-MVIIC reduced the frequency by 35%. These results coupled with the absence of NMDA antagonism by omega-Aga-IVA or omega-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.

Topics: Animals; Calcium Channel Blockers; Cerebral Cortex; Electrophysiology; Epilepsy; Evoked Potentials; In Vitro Techniques; Male; omega-Agatoxin IVA; omega-Conotoxins; Peptides; Rats; Rats, Wistar; Receptors, N-Methyl-D-Aspartate; Spider Venoms; Time Factors