NMDA antagonist blockade of AT8 tau immunoreactive changes in neuronal cultures

被引：9

作者：

Couratier, P ^{[1
]}

Lesort, M ^{[1
]}

Terro, F ^{[1
]}

Dussartre, C ^{[1
]}

Hugon, J ^{[1
]}

机构：

[1] FAC MED LIMOGES,UNITE NEUROBIOL & PATHOL CELLULAIRE,HISTOL LAB,F-87025 LIMOGES,FRANCE

来源：

FUNDAMENTAL & CLINICAL PHARMACOLOGY | 1996年 / 10卷 / 04期

关键词：

tau protein; primary neuronal cultures; NMDA receptor; polyamine site; chronic excitotoxicity;

D O I：

10.1111/j.1472-8206.1996.tb00585.x

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Antagonists at four distinct regulatory sites on the N-methyl-D-aspartate (NMDA) receptor were tested for their ability to attenuate NMDA-mediated chronic excitotoxicity and the consequences on AT8 tau immunoreactivity in neuronal cultures. Excitotoxicity was monitored in cultures by diacetate fluorescein staining. Immunoreactivity of tau phosphorylated at serine 202 was quantified by laser confocal microscopy. The NMDA-receptor antagonists MK801, AP7 and 7-chlorokynurenate significantly blocked NMDA-induced cell death and significantly reduced AT8 tau immunoreactivity. NMDA antagonism by the polyamine site antagonist, ifenprodil, did not completely reverse the increase in AT8 tau immunolabeling induced by NMDA and did not completely protect NMDA-sensitive neurons, suggesting an heterogeneity in the NMDA receptor population.

引用

页码：344 / 349

页数：6

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