Open AccessNebracetam (WEB 1881FU) Prevents N-Methyl-D-Aspartate Receptor-Mediated Neurotoxicity in Rat Striatal Slices
Author(s) -
Yasufumi Kataoka,
Masami Níwa,
Satoshi Koizumi,
Soichi Watanabe,
Masami Kouzuma,
Kohtaro Taniyama
Publication year - 1992
Publication title -
japanese journal of pharmacology/japanese journal of pharmacology
Language(s) - Uncategorized
Resource type - Journals
eISSN - 1347-3506
pISSN - 0021-5198
DOI - 10.1254/jjp.59.247
Subject(s) - nmda receptor , neurotoxicity , dopaminergic , glutamate receptor , neuroprotection , pharmacology , chemistry , dopamine , neuroscience , receptor , biology , medicine , toxicity , biochemistry
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.