GLUTAMATE-INDUCED OVEREXPRESSION OF NMDA RECEPTOR MESSENGER-RNAS AND PROTEIN TRIGGERED BY ACTIVATION OF AMPA/KAINATE RECEPTORS IN RAT HIPPOCAMPUS FOLLOWING FOREBRAIN ISCHEMIA

被引：58

作者：

HEURTEAUX, C

LAURITZEN, I

WIDMANN, C

LAZDUNSKI, M

机构：

[1] Institut de Pharmacologie Moléculaire et Cellulaire, CNRS, 660 route des Lucioles, Sophia Antipolis

来源：

BRAIN RESEARCH | 1994年 / 659卷 / 1-2期

关键词：

IN SITU HYBRIDIZATION; HIPPOCAMPUS; FOREBRAIN ISCHEMIA; GLUTAMATE RECEPTOR;

D O I：

10.1016/0006-8993(94)90864-8

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Severe forebrain ischemia induces a large increase in expression of NMDA receptor subunits in rat brain. One week after ischemia, levels of NMDA-R1 mRNAs in the CA1 pyramidal cells of hippocampus are 7 times higher than those observed in control rats. At 7 days postischemia, an enhanced immunostaining of the NMDA-R1 subunit was observed in all hippocampal structures indicating that changes in mRNA levels are accompanied by changes in receptor protein level. Riluzole, a potent inhibitor of glutamate release and CNQX, a selective AMPA/kainate antagonist, drastically reduced the ischemia-induced expression of mRNAs for the three NMDA receptor subunits while D-AP5, a selective NMDA antagonist, had essentially no effect. Therefore ischemia-induced expression of NMDA receptor subunits is associated with glutamate release and proceeds via an AMPA/kainate pathway. These results together with those of other groups concerning ischemia effects on AMPA and GABA(A) receptor levels, suggest an important role of the induced expression of NMDA receptor subunits in the deleterious effects of ischemia.

引用

页码：67 / 74

页数：8

共 43 条

[31] ANTICONVULSANT AND SLEEP-WAKING INFLUENCES OF RILUZOLE IN A RAT MODEL OF ABSENCE EPILEPSY [J].