Abstract | BACKGROUND AND PURPOSE: METHODS: Adult Sprague-Dawley rats were anesthetized. Inosine, hypoxathine, or vehicle was administered intracerebroventricularly before transient right middle cerebral artery occlusion (MCAo). Animals were placed in behavioral chambers 2 days to 2 weeks after MCAo and then euthanized for tri-phenyl-tetrazolium chloride staining. Glutamate release was measured by microdialysis/high-performance liquid chromatography, and single-unit action potentials were recorded from neurons in the parietal cortex. RESULTS:
Stroke animals receiving inosine pretreatment demonstrated a higher level of locomotor activity and less cerebral infarction. Intracerebroventricular administration of the same dose of hypoxanthine did not confer protection. Coadministration of selective A3 receptor antagonist 3-ethyl-5-benzyl-2-methyl-4-phenylethynyl-6-phenyl-1, 4-(+/-)- dihydropyridine-3,5-dicarboxylate (MRS1191) significantly reduced inosine-mediated protection. Inosine did not alter basal glutamate release, nor did it reduce ischemia-evoked glutamate overflow from cerebral cortex. However, inosine antagonized glutamate-induced electrophysiological excitation in cerebral cortical neurons. CONCLUSIONS:
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Authors | Hui Shen, Guann-Juh Chen, Brandon K Harvey, Paula C Bickford, Yun Wang |
Journal | Stroke
(Stroke)
Vol. 36
Issue 3
Pg. 654-9
(Mar 2005)
ISSN: 1524-4628 [Electronic] United States |
PMID | 15692110
(Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- Hypoxanthines
- Neuroprotective Agents
- Inosine
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Topics |
- Animals
- Brain Ischemia
(etiology, prevention & control)
- Hypoxanthines
(administration & dosage, pharmacology)
- Infarction, Middle Cerebral Artery
(complications, prevention & control)
- Injections, Intraventricular
- Inosine
(administration & dosage, pharmacology)
- Male
- Neuroprotective Agents
(administration & dosage, pharmacology)
- Rats
- Rats, Sprague-Dawley
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