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

Research output: Contribution to journalArticle

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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.

Original languageEnglish
Pages (from-to)791-799
Number of pages9
JournalNeurochemistry International
Volume50
Issue number6
DOIs
Publication statusPublished - 01-05-2007

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Dextromethorphan
Dextrorphan
Neuroprotective Agents
trimethyltin
Anticonvulsants
Hippocampus
Seizures

All Science Journal Classification (ASJC) codes

  • Cellular and Molecular Neuroscience
  • Cell Biology

Cite this

Shin, E. J., Nah, S. Y., Chae, J. S., Bing, G., Shin, S. W., Yen, T. P. H., ... Kim, H. C. (2007). Dextromethorphan attenuates trimethyltin-induced neurotoxicity via σ1 receptor activation in rats. Neurochemistry International, 50(6), 791-799. https://doi.org/10.1016/j.neuint.2007.01.008
Shin, Eun Joo ; Nah, Seung Yeol ; Chae, Jong Seok ; Bing, Guoying ; Shin, Seung Woo ; Yen, Tran Phi Hoang ; Baek, In Hyuk ; Kim, Won Ki ; Maurice, Tangui ; Nabeshima, Toshitaka ; Kim, Hyoung Chun. / Dextromethorphan attenuates trimethyltin-induced neurotoxicity via σ1 receptor activation in rats. In: Neurochemistry International. 2007 ; Vol. 50, No. 6. pp. 791-799.
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Shin, EJ, Nah, SY, Chae, JS, Bing, G, Shin, SW, Yen, TPH, Baek, IH, Kim, WK, Maurice, T, Nabeshima, T & Kim, HC 2007, 'Dextromethorphan attenuates trimethyltin-induced neurotoxicity via σ1 receptor activation in rats', Neurochemistry International, vol. 50, no. 6, pp. 791-799. https://doi.org/10.1016/j.neuint.2007.01.008

Dextromethorphan attenuates trimethyltin-induced neurotoxicity via σ1 receptor activation in rats. / Shin, Eun Joo; Nah, Seung Yeol; Chae, Jong Seok; Bing, Guoying; Shin, Seung Woo; Yen, Tran Phi Hoang; Baek, In Hyuk; Kim, Won Ki; Maurice, Tangui; Nabeshima, Toshitaka; Kim, Hyoung Chun.

In: Neurochemistry International, Vol. 50, No. 6, 01.05.2007, p. 791-799.

Research output: Contribution to journalArticle

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AU - Shin, Eun Joo

AU - Nah, Seung Yeol

AU - Chae, Jong Seok

AU - Bing, Guoying

AU - Shin, Seung Woo

AU - Yen, Tran Phi Hoang

AU - Baek, In Hyuk

AU - Kim, Won Ki

AU - Maurice, Tangui

AU - Nabeshima, Toshitaka

AU - Kim, Hyoung Chun

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N2 - 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.

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