Baclofen does not protect against cerebral ischemia in rats.
Author(s) -
Daniel M. Rosenbaum,
James C. Grotta,
L. Creed Pettigrew,
Peter T. Ostrow,
Roger Strong,
Howard M. Rhoades,
C. M. Picone,
A T Grotta
Publication year - 1990
Publication title -
stroke
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.397
H-Index - 319
eISSN - 1524-4628
pISSN - 0039-2499
DOI - 10.1161/01.str.21.1.138
Subject(s) - medicine , baclofen , ischemia , glutamate receptor , anesthesia , hippocampal formation , pharmacology , nmda receptor , neuroprotection , extracellular , neuronal damage , neuroscience , cardiology , receptor , agonist , biology , biochemistry
Presynaptic release of glutamate into the extracellular compartment and activation of receptor-operated calcium channels may contribute to ischemic neuronal damage. We evaluated the effect of baclofen, a selective inhibitor of presynaptic glutamate release, on mortality, working memory, and light microscopic hippocampal and cortical damage in the four-vessel occlusion model of cerebral ischemia using 64 male Wistar rats. Baclofen (10 mg/kg i.p.) given 1 hour before and 30-60 minutes after 20 minutes of global ischemia did not lessen mortality, prevent ischemic cellular damage, or significantly improve working memory compared with no treatment. We conclude that preischemic and postischemic administration of baclofen does not protect neurons from ischemic injury.
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