Serotonin receptor activation in rats previously deprived of REM sleep.
Pharmacology, biochemistry, and behavior April 1, 1983 DOI: 10.1016/0091-3057(83)90271-x (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Experimental study Peer reviewed |
|---|---|
| Population | 3 day REM-deprived or control rats |
| Interventions | L-5-hydroxytryptophan L-tryptophan MAO inhibitors quipazine 5-methoxy-N |
| Dose | MeO-DMT 0.75-6.0 mg/kg; quipazine 0.3-1.25 mg/kg and 2.4-6.0 mg/kg |
| Duration | 3 day REM sleep deprivation |
| Topics | Serotonin |
| Citations | 25 |
| Key findings | REM sleep deprivation increased rats' responsiveness to serotonin precursors but reduced responsiveness to low doses of quipazine, suggesting altered serotonin turnover and receptor sensitivity. |
Abstract
The effects of serotonin precursors (L-5-hydroxytryptophan and L-tryptophan, with or without MAO inhibitors) and of agonists (quipazine and 5-methoxy-N,N-dimethyltryptamine-MeO-DMT) were studied in 3 day REM-deprived or control rats, by recording the presence of the serotonin syndrome and the number of head shakes. The REM sleep-deprived rats showed a larger incidence of the serotonin syndrome and a greater number of head shakes in comparison to the control animals, when challenged with the serotonin precursors. Conversely, REM sleep deprivation did not modify the responsiveness of rats to 0.75-6.0 mg/kg of MeO-DMT and to 2.4-6.0 mg/kg of quipazine. However, REM-deprived rats reacted less than controls to 0.3-1.25 mg/kg of quipazine. Increased turnover due to REM sleep deprivation could explain the augmented responsiveness of the rats to the serotonin precursors. Conversely, the decreased responsiveness to quipazine could result from receptor hyposensitivity due to intense receptor activation, caused by the increased turnover, during the 3 day period of REM sleep deprivation.