Baclofen does not protect against cerebral ischemia in rats
Autor: | James C. Grotta, C M Picone, A T Grotta, P. Ostrow, Howard M. Rhoades, L C Pettigrew, Roger Strong, D M Rosenbaum |
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Rok vydání: | 1990 |
Předmět: |
Male
Baclofen Ischemia Hippocampus Motor Activity Hippocampal formation Pharmacology Brain Ischemia chemistry.chemical_compound Reference Values medicine Extracellular Animals Advanced and Specialized Nursing Dose-Response Relationship Drug Voltage-dependent calcium channel business.industry Glutamate receptor Rats Inbred Strains medicine.disease Rats medicine.anatomical_structure nervous system chemistry Cerebral cortex Anesthesia Neurology (clinical) Cardiology and Cardiovascular Medicine business |
Zdroj: | Stroke. 21:138-140 |
ISSN: | 1524-4628 0039-2499 |
DOI: | 10.1161/01.str.21.1.138 |
Popis: | 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. |
Databáze: | OpenAIRE |
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