N-[1-(2-THIENYL)CYCLOHEXYL]-PIPERIDINE (TCP) DOES NOT BLOCK KAINIC ACID-INDUCED STATUS EPILEPTICUS BUT REDUCES SECONDARY HIPPOCAMPAL DAMAGE

被引：36

作者：

LERNERNATOLI, M ^{[1
]}

RONDOUIN, G ^{[1
]}

BELAIDI, M ^{[1
]}

BALDYMOULINIER, M ^{[1
]}

KAMENKA, JM ^{[1
]}

机构：

[1] ECOLE NATL SUPER CHIM,F-34075 MONTPELLIER,FRANCE

来源：

NEUROSCIENCE LETTERS | 1991年 / 122卷 / 02期

关键词：

STATUS EPILEPTICUS; KAINIC ACID; HIPPOCAMPUS; NMDA; NEUROPROTECTION; TCP;

D O I：

10.1016/0304-3940(91)90851-J

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Distant damage, localized in the CA3 and CA1 areas, was observed in the hippocampus of rats as a consequence of status epilepticus (SE) induced by the injection of 2.5 nmol of kainic acid (KA) into the amygdala. In animals pretreated with an intraperitoneal injection of the non-competitive antagonist of the N-methyl-D-aspartate receptor, N-[1-(2-thienyl)cyclohexyl]-piperidine (TCP) (20 mg/kg), distant neuronal damage was reduced (CA1 neurons were always spared) whereas the rats still developed SE with an earlier onset. These results demonstrate the protective effect of TCP and confirm that epileptic activity and brain damage may be dissociated by NMDA receptor antagonists.

引用

页码：174 / 178

页数：5

共 20 条

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