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.
journal_name
Neurochem Intjournal_title
Neurochemistry internationalauthors
Shin EJ,Nah SY,Chae JS,Bing G,Shin SW,Yen TP,Baek IH,Kim WK,Maurice T,Nabeshima T,Kim HCdoi
10.1016/j.neuint.2007.01.008subject
Has Abstractpub_date
2007-05-01 00:00:00pages
791-9issue
6eissn
0197-0186issn
1872-9754pii
S0197-0186(07)00038-1journal_volume
50pub_type
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