Title |
Kinin-B2 Receptor Mediated Neuroprotection after NMDA Excitotoxicity Is Reversed in the Presence of Kinin-B1 Receptor Agonists
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Published in |
PLOS ONE, February 2012
|
DOI | 10.1371/journal.pone.0030755 |
Pubmed ID | |
Authors |
Antonio H. Martins, Janaina M. Alves, Dinely Perez, Marimeé Carrasco, Wilmarie Torres-Rivera, Vesna A. Eterović, Pedro A. Ferchmin, Henning Ulrich |
Abstract |
Kinins, with bradykinin and des-Arg(9)-bradykinin being the most important ones, are pro-inflammatory peptides released after tissue injury including stroke. Although the actions of bradykinin are in general well characterized; it remains controversial whether the effects of bradykinin are beneficial or not. Kinin-B2 receptor activation participates in various physiological processes including hypotension, neurotransmission and neuronal differentiation. The bradykinin metabolite des-Arg(9)-bradykinin as well as Lys-des-Arg(9)-bradykinin activates the kinin-B1 receptor known to be expressed under inflammatory conditions. We have investigated the effects of kinin-B1 and B2 receptor activation on N-methyl-D-aspartate (NMDA)-induced excitotoxicity measured as decreased capacity to produce synaptically evoked population spikes in the CA1 area of rat hippocampal slices. |
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Mendeley readers
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Student > Master | 6 | 15% |
Researcher | 4 | 10% |
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Sports and Recreations | 1 | 2% |
Other | 2 | 5% |
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