Dextromethorphan inhibits 5-hydroxytryptamine uptake by human blood platelets and decreases 5-hydroxyindoleacetic acid content in rat brain
Liisa Ahtee
Journal of Pharmacy and Pharmacology March 1, 1975 DOI: 10.1111/j.2042-7158.1975.tb09433.x (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Experimental study Peer reviewed |
|---|---|
| Population | Human blood platelets and rat brain |
| Interventions | Dextromethorphan imipramine methadone probenecid pargyline |
| Dose | 120 nM; 20 to 40 mg kg−1 |
| Key findings | Dextromethorphan inhibited platelet serotonin uptake with a 50% inhibitory concentration of 120 nM, less potent than imipramine (22 nM) but more potent than methadone (590 nM). In rats, dextromethorphan (20-40 mg/kg) time- and dose-dependently decreased brain 5-HIAA and probenecid-induced 5-HIAA accumulation, without altering pargyline-induced changes. The authors suggest these effects may arise from inhibition of serotonin reuptake into neurons. |
Abstract
Abstract: The effect of dextromethorphan on the uptake and metabolism of 5-hydroxytryptamine (5-HT) was studied in human blood platelets and in rat brain. In the concentration of 120 nM dextromethorphan inhibited the uptake of 5-HT (1 μM) into platelets by 50%. The corresponding concentrations of imipramine and methadone under similar conditions were 22 and 590 nM, respectively. Dextromethorphan (20 to 40 mg kg−1) decreased the concentration of brain 5-hydroxyindoleacetic acid (5-HIAA) and the probenecid-induced accumulation of 5-HIAA time- and dose-dependently. However, dextromethorphan did not alter the pargyline-induced changes in brain 5-HT metabolism. Dextromethorphan-induced changes in brain 5-HT metabolism could arise from the inhibition of the reuptake of 5-HT into neurons.