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Title

A(2A) adenosine receptor deficiency attenuates brain injury induced by transient focal ischemia in mice

AuthorsChen, J. F.; Huang, Z.; Ma, J.; Zhu, J.; Moratalla, Rosario ; Standaert, D.; Moskowitz MA; Fink, J. S,; Schwarzschild, M. A.
KeywordsA2A adenosine receptor, ischemi, astrokepurine, receptorknock-outneuroprotection
Issue Date1999
PublisherSociety for Neuroscience
CitationJournal of Neuroscience 19: 9192- 9200 (1999)
AbstractExtracellular adenosine critically modulates ischemic brain injury, at least in part through activation of the A(1) adenosine receptor. However, the role played by the A(2A) receptor has been obscured by intrinsic limitations of A(2A) adenosinergic agents. To overcome these pharmacological limitations, we explored the consequences of deleting the A(2A) adenosine receptor on brain damage after transient focal ischemia. Cerebral morphology, as well as vascular and physiological measures (before, during, and after ischemia) did not differ between A(2A) receptor knock-out and wild-type littermates. The volume of cerebral infarction, as well as the associated neurological deficit induced by transient filament occlusion of the middle cerebral artery, were significantly attenuated in A(2A) receptor knock-out mice. This neuroprotective phenotype of A(2A) receptor-deficient mice was observed in different genetic backgrounds, confirming A(2A) receptor disruption as its cause. Together with complimentary pharmacological studies, these data suggest that A(2A) receptors play a prominent role in the development of ischemic injury within brain and demonstrate the potential for anatomical and functional neuroprotection against stroke by A(2A) receptor antagonists
URIhttp://hdl.handle.net/10261/150792
Identifiersissn: 0270-6474
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