Lysergic acid diethylamide: evidence for stimulation of cerebral dopamine receptors
M. Da Prada, A. Saner, W.p. Burkard, G. Bartholini, A. Pletscher
Brain Research August 1, 1975 DOI: 10.1016/0006-8993(75)90877-x via OpenAlex
Summary
AI-generated from the abstractLysergic acid diethylamide (LSD) stimulates dopamine receptors in the central nervous system, which may contribute to LSD-induced psychosis. In rats, LSD decreased striatal and retinal homovanillic acid levels without changing dopamine levels, but delayed the disappearance of dopamine after a-methyl-p-tyrosine treatment. In cats, LSD reduced dopamine output into the caudate nucleus perfusate. Additionally, LSD increased adenylate cyclase activity in rat striatal homogenates. These findings suggest that dopamine receptor stimulation is involved in the effects of LSD.
Study at a glance
| Characteristics | Experimental study Peer reviewed |
|---|---|
| Population | Rats and cats |
| Intervention | Lysergic acid diethylamide (LSD) |
| Topics | LSD |
| Keywords | Homovanillic acid Caudate nucleus Stimulation Dopamine receptor |
| Citations | 71 |
| Key finding | LSD stimulates dopamine receptors in the central nervous system, which may be involved in LSD-induced psychosis. |
Abstract
In the rat, lysergic acid diethylamide (LSD) decreased the striatal and retinal content of homovanillic acid. LSD did not change the level of dopamine (DA), but delayed the a-methyl-p-tyrosine-induced disappearance of this amine in the teldiencephalon. In the cat, LSD diminished the DA output into the perfusate of the caudate nucleus. Furthermore, LSD increased the activity of adenylate cyclase in striatal homogenates of rat. These and other findings indicate that in the central nervous system LSD stimulates DA receptors which may be involved in LSD-induced phychosis.