Abstract
D-Lysergic acid diethylamide (LSD) given pareriterally produces a reversible cessation of the spontaneous activity of neuronal units in the midbrain raphe nuclei of the rat1. Threshold doses of LSD required to produce this effect are extremely small in relation to those typically used in rats (10–20 µg/kg, intravenously). Substances the behavioural effects of which are similar to those of LSD (for example, N,N-dimethyltryptamine and mescaline) also inhibit raphe units, although none is as potent as LSD2. A variety of other types of drugs (for example, atropine, phencyclidine, chlorpromazine) do not affect the activity of raphe units2. The inhibitory effect of LSD is specific for units in the dorsal and median raphe nuclei; in other mid-brain areas (for example, reticular formation), the drug either has no effect or accelerates unit activity1. According to the fluorescence histochemical method the midbrain raphe nuclei are comprised of serotonin-containing neurones3. Axons of the raphe neurones supply the principal serotonin input to the forebrain4. Large doses of LSD induce a prolonged inhibition of the serotonin-containing neurones1; this inhibition may account for the reduced metabolism of brain serotonin observed after injections of LSD5–8.
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FOOTE, W., SHEARD, M. & AGHAJANIAN, G. Comparison of Effects of LSD and Amphetamine on Midbrain Raphe Units. Nature 222, 567–569 (1969). https://doi.org/10.1038/222567a0
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DOI: https://doi.org/10.1038/222567a0
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