Glutamate N-methyl-D-aspartate receptor blockade prevents induction of GAP-43 after focal ischemia in rats.

Abstract:

:Growth associated protein-43 (GAP-43) gene induction may be involved in reactive events that follow cerebral ischemic damage. Antagonists of the N-methyl-D-aspartate (NMDA) subclass of glutamate receptors are thought to ameliorate functional outcome after ischemic injury. To assess whether glutamate NMDA receptor blockade could alter GAP-43 postischemic induction we performed immunocytochemistry in rat brains that had been subjected to middle cerebral artery occlusion. Cortical cells did not constitutively express GAP-43, yet focal ischemia induced its expression, with an intense signal generated in cells over the lesioned area at 6 h, increasing at 24 h postischemia. This signal was effectively decreased by pretreatment with the NMDA receptor antagonist (5R,10S)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]-cyclohepten-5,10-imine hydrogen maleate (0.1 mg/kg s.c.), but not by the glutamate release blocker riluzole (8 mg/kg i.v.), suggesting that overactivation of NMDA receptor during ischemia is linked to GAP-43 expression.

journal_name

Neurosci Lett

journal_title

Neuroscience letters

authors

Luque JM,Puig N,Martínez JM,González-García C,Ceña V

doi

10.1016/s0304-3940(01)01833-x

keywords:

subject

Has Abstract

pub_date

2001-06-08 00:00:00

pages

87-90

issue

2

eissn

0304-3940

issn

1872-7972

pii

S030439400101833X

journal_volume

305

pub_type

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