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

Eun Joo Shin, 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

研究成果: Article査読

39 被引用数 (Scopus)

抄録

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.

本文言語English
ページ(範囲)791-799
ページ数9
ジャーナルNeurochemistry International
50
6
DOI
出版ステータスPublished - 05-2007
外部発表はい

All Science Journal Classification (ASJC) codes

  • 細胞および分子神経科学
  • 細胞生物学

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