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Drugs that activate the 5-HT2A receptor no longer substitute in these ‘‘LSD-90’’ animals; rather, DA D2-like agonists such as apomorphine fully substitute, and this cue is blocked by D2 antagonists such as haloperidol. This effect is not seen in DOI-trained rats, where the cue is mediated through 5-HT2A receptors irrespective of the pretreatment time. The most likely explanation for this finding is that LSD has significant affinity for DA receptors, whereas none of the other hallucinogens possess that pharmacology.

J. (1999c). Serotonin-glutamate interactions: a new target for antipsychotic drugs. Neuropsychopharmacology 21, S122 – S133. Aghajanian, G. , Foote, W. , & Sheard, M. H. (1968). Lysergic acid diethylamide: sensitive neuronal units in the midbrain raphe. Science 161, 706 – 708. Aghajanian, G. , Foote, W. , & Sheard, M. H. (1970). Action of psychotogenic drugs on single midbrain raphe neurons. J Pharmacol Exp Ther 171, 178 – 187. Aghajanian, G. , Haigler, H. , & Bloom, F. E. (1972). Lysergic acid diethylamide and serotonin: direct actions on serotonin-containing neurons in rat brain.

2002). Thus, effective doses of hallucinations may provide excessive stimulation of 5-HT2A receptors in PFC, leading to speculation that perhaps subhallucinogenic dosages of 5-HT2A agonists might facilitate working memory. The studies of indirect semantic priming by Spitzer et al. (1996) cited earlier show yet another effect of 5-HT2A receptor activation on cognition. No doubt there are many cognitive tasks that will be affected by hallucinogens based on what we are now learning about the anatomical locations and functions of the 5-HT2A receptor.

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