Action of hallucinogens on raphe-evoked dorsal root potentials (DRPs) in the cat.
Pharmacology, biochemistry, and behavior February 1, 1986 DOI: 10.1016/0091-3057(86)90364-3 via PubMed
Summary
AI-generated from the abstractA single low dose of LSD potentiates the dorsal root potential (DRP) evoked by stimulation of the inferior central nucleus in cats, whereas 5-MeODMT, ketamine, and PCP inhibit it. Tolerance develops to LSD's facilitatory effect but not to 5-MeODMT's inhibition, and ketamine's effect does not produce tachyphylaxis. The raphe-evoked DRP, traditionally thought to be serotonin-mediated, may actually involve a non-serotonergic transmitter, as tryptophan and fluoxetine do not potentiate it, and it resists blockade by serotonin-depleting agents.
Study at a glance
| Characteristics | Experimental study Peer reviewed |
|---|---|
| Population | Cats |
| Interventions | LSD 5-methoxy-N N-dimethyltryptamine (5-MeODMT) ketamine phencyclidine (PCP) tryptophan fluoxetine parachlorophenylalanine reserpine 5 7-dihydroxytryptamine |
| Key finding | The raphe-evoked dorsal root potential may be mediated at least in part by a non-serotonergic transmitter. |
Abstract
The dorsal root potential (DRP) evoked by stimulation of the inferior central nucleus (ICN) of the cat is affected by administration of a variety of hallucinogenic agents. It has been previously shown that a single low dose of LSD is unique in that it potentiates this DRP, while injections of 5-methoxy-N,N- dimethyltryptamine (5-MeODMT), ketamine or phencyclidine (PCP) inhibit its production. Tolerance develops to the facilitatory effect of low doses of LSD on the DRP, but not to the inhibitory action of 5-MeODMT. Repeated injections of ketamine every 30 minutes also fail to produce tachyphylaxis to the inhibitory effect of this dissociative anesthetic. The raphe-evoked DRP is a long latency potential that is inhibited by a wide variety of putative serotonin antagonists and has therefore been traditionally thought to be mediated by serotonin. However, in light of the inability of either tryptophan or fluoxetine to potentiate this DRP, and the resistance of this DRP to blockade by parachlorophenylalanine, reserpine or intrathecally administered 5,7-dihydroxytryptamine, it appears that this potential may in fact be mediated, at least in part, by a non-serotonergic transmitter.