1994
DOI: 10.1097/00000542-199408000-00026
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Dextromethorphan Inhibits Ischemia-induced c-fos  Expression and Delayed Neuronal Death in Hippocampal Neurons

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Cited by 33 publications
(14 citation statements)
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“…DMO has recently been described as potentially neuroprotective. 41,42 Neuroprotection appears to be linked to N-methyl-D-aspartate receptor blockade, which was shown to be a property of DOP. 43 DMO also exhibits anticonvulsant activity and it has been suggested that this eect results primarily from metabolism of DMO to its active metabolite DOP.…”
Section: Discussionmentioning
confidence: 99%
“…DMO has recently been described as potentially neuroprotective. 41,42 Neuroprotection appears to be linked to N-methyl-D-aspartate receptor blockade, which was shown to be a property of DOP. 43 DMO also exhibits anticonvulsant activity and it has been suggested that this eect results primarily from metabolism of DMO to its active metabolite DOP.…”
Section: Discussionmentioning
confidence: 99%
“…It can attenuate the glutamate-induced neurotoxicity and has a neuroprotective property against the ischemia-induced brain damage [8]. Dextromethorphan has many other medical applications, such as pain relief, psychological application, and the treatment of addiction [9].…”
Section: Discussionmentioning
confidence: 99%
“…The results of numerous in vivo and in vitro studies have shown that induction of c-Fos protein precedes neuronal death and participates in neuronal injury after ischemia [14]. Likewise Renexin®, the dextromethorphan, a neuroprotective drug, reduced an expression of c-Fos protein one hour after ischemia, and also protected delayed neuronal degeneration in the CA 1 region of the hippocampus [15,16]. These results suggest that reduction of c-Fos expression one hour after ischemia may be positively correlated with survival of neurons.…”
Section: +mentioning
confidence: 99%