The effect of Toki-Shakuyaku-San (TJ-23) was examined on various models of brain damage in uitro. TJ-23 (10 mg/mL) significantly protected striatal slices from dysfunction induced by high K + and BAY K-8644 but not from that by L-glutamate and N-methyl-D-aspartate, an effect which was similar to that of nifedipine, a CazC antagonist. The present findings, therefore, raised the possibility that TJ-23 expressed a neuroprotective action on hypoxidischaemia-induced brain damage by inhibiting an excess Ca2+ entry through voltage-gated Ca2+ channels.

ABSTRACT-The effects of nebracetam were investigated on N-methyl-D-aspartate (NMDA) receptor and voltage-operated Ca 2+ channels (VOCC)-mediated neural dysfunction by directly monitoring the real-time dynamics of dopamine released from rat striatal slices. Nebracetam (105 and 10-4 M) com pletely protected against striatal dopaminergic impairment induced by L-glutamate and NMDA, respec tively. 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 Ca 2+ channels.

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