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Sloviter RS, Drust EG, Damiono BP, Connor JB. 
“Serotonergic Mediation Of Behavioral Effects In Rats Of Indoles And Phenethylamine Hallucinogens”. 
Federation Proc.. 1980;39(3, Part I):608.
A rat behavioral model of central serotonin (5-HT) receptor activation in vivo (Sloviter et. al., JPET, 206:339, 1978) was utilized to study hallucinogens. Lysergids (LSD), N,N-dimethyltryptamine (DMT), N,N-diethyltryptamine (DET), 5-methoxy-N,N-dimethyltrypLamine (5-MeODMT) ibogaine (IBO), mescaline (MES), methoxyamphetamine (PMA), 3,4,5-trimethoxyamphetomine (TMA), 2,5-dimethoxy-4-methylamphetamine (DMA) 2,5-dimethoxy-4-bromoamphetamine (DOB), and 3,4-dimethoxyphenethylamine (DMPEA) caused the 5-HT behavioral syndrome. The potency rank (LSD > 5-MeODMT > DET = DOB PMA > DOM = DMT = IBO > DMA > TMA > mescaline > DMPEA ) correlates well with hallucinogenic potency in man. Bromo-LSD, a non-hallucinogenic congener of LSD that attenuates LSD hallucinations in man did not cause the 5-HT syndrome, but rather, blocked the syndromes caused by all eleven hallucinogens. Studies on mechanisms of action show that all hallucinogens except PEA activate 5-HT receptors directly. PMA releases endogenous 5-HT. 5-MeODMT dose-response curves were used to test the 5-HT agonist vs. antagonist properties of low doses of LSD (10 and 100 mcg/kg). Results show that over range, LSD is a 5-HT agonist. We conclude that in phenethylamine hallucinogens share a common action of central 5-HT receptors.
Notes # : Abstr. No. 1815
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