Role of the excitotoxic mechanism in the development of neuronal damage following repeated brief cerebral ischemia in the gerbil: protective effects of MK-801 and pentobarbital.

Pretreatment with MK-801 (an NMDA antagonist) or pentobarbital (a GABAA receptor-effector) ameliorated histopathological neuronal damage to the hippocampal CA1 subfield and to the thalamus following three 2-min forebrain ischemia at 1-h intervals in the gerbil. Flunarizine, a calcium antagonist, failed to prevent the neuronal damage. The results suggest that the excitotoxic mechanism plays a role in the neuronal damage following repeated ischemia.