Abstract
The effects of nebracetam were investigated on N-methyl-D-aspartate (NMDA) receptor- and voltage-operated Ca2+ channels (VOCC)-mediated neural dysfunction by directly monitoring the real-time dynamics of dopamine released from rat striatal slices. Nebracetam (10-5 and 10-4 M) completely protected against striatal dopaminergic impairment induced by L-glutamate and NMDA, respectively. BAY K-8644-evoked striatal dysfunction was not blocked by nebracetam (10-4 M). Therefore, nebracetam seems to produce a neuroprotective action by interacting, at least in part, with NMDA receptor-operated Ca2+ channels.