| Literature DB >> 17386960 |
Eun-Joo Shin1, Seung-Yeol Nah, Jong Seok Chae, Guoying Bing, Seung Woo Shin, Tran Phi Hoang Yen, In-Hyuk Baek, Won-Ki Kim, Tangui Maurice, Toshitaka Nabeshima, Hyoung-Chun Kim.
Abstract
We showed that dextromethorphan (DM) provides neuroprotective/anticonvulsant effects and that DM and its major metabolite, dextrorphan, have a high-affinity for sigma(1) receptors, but a low affinity for sigma(2) receptors. In addition, we found that DM has a higher affinity than DX for sigma(1) 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 sigma(1) receptor antagonist BD 1047, but not by the sigma(2) receptor antagonist ifenprodil. DM attenuates TMT-induced reduction in the sigma(1) 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 sigma(1) receptor stimulation.Entities:
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Year: 2007 PMID： 17386960 DOI： 10.1016/j.neuint.2007.01.008
Source DB: PubMed Journal: Neurochem Int ISSN： 0197-0186 Impact factor: 3.921