Induction of phencyclidine-like behavior in rats by dextrorphan but not dextromethorphan.
J I Székely, L G Sharpe, J H Jaffe
Pharmacology, biochemistry, and behavior October 1991 DOI: 10.1016/0091-3057(91)90569-n (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Animal behavioral pharmacology experiment Peer reviewed |
|---|---|
| Population | Rats |
| Interventions | Dextromethorphan Dextrorphan Phencyclidine |
| Dose | DO 15-120 mg/kg; DM 15-120 mg/kg; PCP 1.25-20 mg/kg; PCP 10 mg/kg for interaction tests |
| Key findings | Dextrorphan produced PCP-like dose-dependent hyperactivity, stereotypy, and ataxia in rats, whereas dextromethorphan produced only moderate hyperactivity at higher doses. Dextrorphan facilitated PCP-induced hyperactivity while dextromethorphan dose-dependently inhibited it. The authors propose that DM abuse in humans may reflect its conversion to dextrorphan, a metabolite with PCP-like effects. |
Abstract
The behavioral effects of dextromethorphan (DM), dextrorphan (DO) and phencyclidine (PCP) were compared in rats. DO (15-120 mg/kg) was similar to PCP (1.25-20 mg/kg) in inducing dose-dependent locomotor hyperactivity, stereotypy and ataxia. DM (15-120 mg/kg) induced moderate hyperactivity only at the higher doses about 45 min after treatment. DM and DO modified the locomotor facilitation induced by 10 mg/kg PCP in opposite directions. Pretreatment with DO facilitated, whereas DM dose-dependently inhibited PCP-elicited hyperactivity. Although the metabolism of DM in rats is unknown, the recently reported abuse of DM in humans may occur by its conversion to DO in the organism, i.e., to a metabolite which produces PCP-like effects.