Neurotoxicity of dextrorphan

Genaro G. Ortiz, Juan M. Guerrero, Russel J. Reiter, Burkhard H. Poeggeler, Oscar K. Bitzer-Quintero, Alfredo Feria-Velasco

Research output: Contribution to journalArticlepeer-review

3 Scopus citations


Background. The noncompetitive NMDA antagonists phencyclidine (PCP) and dizocilpine (MK-801) have been considered for use as neuroprotective therapeutic agents, although both produce injury in neurons of cingulate and retrosplenial cortices in rodents. The low-affinity, noncompetitive NMDA antagonist dextrorphan has been considered for use as a neuroprotective therapeutic drug. The aim of the present work was to evaluate the neurotoxicity of dextrorphan. Methods. Sprague-Dawley male rats were used and injected with either saline or dextrorphan (30 mg/kg i.p.). The animals were sacrificed 30 min later, and the brain was examined for histopathological changes. Results. After systemic administration of the drug, hyperchromatic and shrunken nuclei with chromatin condensation and disruption were observed. Also, granular and vacuolated cytoplasm was apparent in pyramidal neurons in the retrosplenial (posterior cingulate) cortex. Status spongiosus (spongy degeneration) of the neuropil was also detected. Conclusions. Morphological changes are similar to those described previously, which are induced by high-affinity, noncompetitive NMDA antagonists, such as MK-801.

Original languageEnglish (US)
Pages (from-to)125-127
Number of pages3
JournalArchives of Medical Research
Issue number2
StatePublished - Mar 1999


  • Dextrorphan
  • NMDA antagonists
  • Neurotoxicity
  • Posterior cingulate cortex

ASJC Scopus subject areas

  • General Medicine


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