A(2A) adenosine receptor deficiency attenuates brain injury induced by transient focal ischemia in mice.
J Neurosci
; 19(21): 9192-200, 1999 Nov 01.
Article
em En
| MEDLINE
| ID: mdl-10531422
ABSTRACT
Extracellular 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.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Encéfalo
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Ataque Isquêmico Transitório
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Circulação Cerebrovascular
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Receptores Purinérgicos P1
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Lesão Encefálica Crônica
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Hemodinâmica
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Atividade Motora
Tipo de estudo:
Etiology_studies
Limite:
Animals
Idioma:
En
Revista:
J Neurosci
Ano de publicação:
1999
Tipo de documento:
Article
País de afiliação:
Estados Unidos