Induction of heat shock protein HSP-70 in rat retrosplenial cortex following administration of dextromethorphan

K Hashimoto; S Tomitaka; N Narita; Y Minabe; M Iyo; S Fukui

doi:10.1016/1382-6689(96)00016-6

Induction of heat shock protein HSP-70 in rat retrosplenial cortex following administration of dextromethorphan

Environ Toxicol Pharmacol. 1996 Jul 15;1(4):235-9. doi: 10.1016/1382-6689(96)00016-6.

Authors

K Hashimoto¹, S Tomitaka, N Narita, Y Minabe, M Iyo, S Fukui

Affiliation

¹ Division of Cortical Function Disorder, National Institute of Neuroscience, National Center of Neurology and Psychiatry (NCNP), Kodaira, Tokyo 187, Japan; Division of Drug Dependence and Psychotropic Clinical Research, National Institute of Mental Health, NCNP, Ichikawa, Chiba 272, Japan.

PMID: 21781688
DOI: 10.1016/1382-6689(96)00016-6

Abstract

Dextromethorphan, a non-competitive antagonist of N-methyl-d-aspartate (NMDA) receptor, is one of the most widely used non-opioid cough suppressants, and it is generally considered to be a safe drug. In this study, we have examined whether dextromethorphan is neurotoxic to rat cerebrocortical neurons. Induction of heat shock protein HSP-70, an indicator of cellular stress, was observed in the posterior cingulate and retrosplenial cortex of rat brain after a single administration of dextromethorphan (75 mg/kg). Furthermore, administration of dextromethorphan (75 mg/kg) caused vacuolization in the same regions. These results suggest that high doses of dextromethorphan could cause neuronal injury in the cerebrocortical neurons.