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Dextromethorphan attenuates trimethyltin-induced neurotoxicity via σ1 receptor activation in rats

Title
Dextromethorphan attenuates trimethyltin-induced neurotoxicity via σ1 receptor activation in rats
Authors
Shin E.-J.Nah S.-Y.Chae J.S.Bing G.Shin S.W.Yen T.P.H.Baek I.-H.Kim W.-K.Maurice T.Nabeshima T.Kim H.-C.
Ewha Authors
김원기
Issue Date
2007
Journal Title
Neurochemistry International
ISSN
0197-0186JCR Link
Citation
vol. 50, no. 6, pp. 791 - 799
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
We showed that dextromethorphan (DM) provides neuroprotective/anticonvulsant effects and that DM and its major metabolite, dextrorphan, have a high-affinity for σ1 receptors, but a low affinity for σ2 receptors. In addition, we found that DM has a higher affinity than DX for σ1 sites, whereas DX has a higher affinity than DM for PCP sites. We extend our earlier findings by showing that DM attenuated trimethyltin (TMT)-induced neurotoxicity (convulsions, hippocampal degeneration and spatial memory impairment) in rats. This attenuation was reversed by the σ1 receptor antagonist BD 1047, but not by the σ2 receptor antagonist ifenprodil. DM attenuates TMT-induced reduction in the σ1 receptor-like immunoreactivity of the rat hippocampus, this attenuation was blocked by the treatment with BD 1047, but not by ifenprodil. These results suggest that DM prevents TMT-induced neurotoxicity, at least in part, via σ1 receptor stimulation. © 2007 Elsevier Ltd. All rights reserved.
DOI
10.1016/j.neuint.2007.01.008
Appears in Collections:
자연과학대학 > 화학·나노과학전공 > Journal papers
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