GLYCINE ANTAGONISM DOES NOT BLOCK ISCHEMIC SPONTANEOUS DEPOLARIZATIONIN THE RAT

THIS study examined the effect of glycine recognition site antagonism (ACEA 1021) on the incidence of spontaneous depolarizations in the pen umbra of a focal ischemic lesion. Rats were administered either vehicl e (n = 7), ACEA 1021 (n = 7) or dizocilpine (n = 5) and then underwent 90 min middle cerebral artery occlusion. The cortical direct current (DC) potential was recorded. During ischemia, 7 +/- 3 DC shifts occurr ed in the vehicle group. ACEA 1021 did not reduce this frequency (7 +/ - 2 DC shifts) although dizocilpine did (1 +/- 1 DC shifts; p = 0.02). The previously demonstrated neuroprotective property of ACEA 1021 dur ing focal cerebral ischemia cannot be attributed to reduction of spont aneous depolarization in the ischemic penumbra.