期刊
NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY
卷 380, 期 3, 页码 223-232出版社
SPRINGER
DOI: 10.1007/s00210-009-0426-8
关键词
A(2A) receptor knockout mice; Pentylenetetrazol; Pilocarpine; Kindling; Convulsants
资金
- Fondation Medicale Reine Elisabeth
- Interuniversity Attraction Poles Programme [P6-14]
- Actions de Recherche Concertees of the Communaute Francaise de Belgique
- Fonds de la Recherche Scientifique Medicale of Belgium
- Belgian Fonds National de la Recherche Scientifique
The neuromodulator adenosine, acting through activation of four defined metabotropic receptors called A(1), A(2A), A(2B) and A(3,) has been proposed as an endogenous anticonvulsant. Here, the consequences of deleting the adenosine A(2A) receptor have been examined in different experimental models of epilepsy. A(2A)R KO mice were not protected against seizures originating from brainstem structures, namely electroshock-induced seizures. The intensities of seizures induced by pentylenetetrazol or pilocarpine, as well as the percentages of convulsing mice, were significantly reduced in A(2A) receptor knockout (A(2A)R KO) animals. A(2A)R KO mice exhibited reduced pentylenetetrazol-induced kindled seizures, demonstrating an important role of the A(2A) receptor in the acquisition of kindling. These data suggest that adenosine stimulating A(2A) receptors modulates excitatory neurotransmission and exacerbates limbic seizures. It is therefore suggested that adenosine A(2A) receptor antagonists might offer protection from some epileptic syndromes.
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