Nociception is enhanced after low doses and reduced after high doses of the serotonin receptor agonist 5-methoxy-N,N-dimethyltryptamine.
Neuroscience letters September 1, 1980 DOI: 10.1016/0304-3940(80)90198-6 via PubMed
Summary
AI-generated from the abstractInjecting 5-methoxy-N,N-dimethyltryptamine into the brain's ventricles altered pain sensitivity in rats, measured by the tail-flick test. Low doses (1.6 to 25 micrograms) reduced tail-flick latencies by 13-24%, indicating hyperalgesia (increased pain sensitivity), likely from decreased activity in descending serotonergic neurons. Moderate doses (50 and 100 micrograms) produced a biphasic response: initial hyperalgesia followed by analgesia. The highest dose (400 micrograms) increased latencies by 28-39%, indicating analgesia, probably by stimulating spinal postsynaptic serotonergic receptors.
Study at a glance
| Characteristics | Experimental study Peer reviewed |
|---|---|
| Sample size | 48 |
| Population | Rats |
| Intervention | N-dimethyltryptamine |
| Dose | 1.6, 3.1, 6.3, 12.5, 25, 50, 100, and 400 micrograms |
| Citations | 34 |
| Key finding | Low doses of intracerebroventricular 5-methoxy-N,N-dimethyltryptamine cause hyperalgesia, while high doses cause analgesia, with biphasic effects at intermediate doses. |
Abstract
The effects on pain sensitivity of intracerebroventricular injections of 5-methoxy-N,N-dimethyltryptamine were tested by the tail-flick method. Following administration of 1.6, 3.1, 6.3, 12.5 and 25 micrograms (n = 8 for each dose), tail-flick latencies were reduced by 13-24%. Fifty and 100 micrograms caused a biphasic response (hyperalgesia followed by analgesia), whereas 400 micrograms increased mean latencies by 28-39%. The hyperalgesia observed after low doses was most likely due to reduced activity in descending serotonergic neurons following presynaptic stimulation. Higher doses caused analgesia, probably by stimulating spinal postsynaptic serotonergic receptors as well.