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Freedman DX. 
“LSD, Psychotogenic Procedures, and Brain Neurohumors.”. 
Psychopharmacol Bull. 1975;11(2):42-43.
The effects of LSD on brain neurohumors have been investigated using rats, mice, cats, rabbits and monkeys. LSD-induced increase in brain serotonin in-vivo has been localized subcellularly in the synaptic vesicle fraction. Reserpine pretreatment abolishes this increase. Loss of body weight was an accurate predictor of degree of reserpinization and there was significant correlation between % weight loss and degree of 5-HT depletion and 5-HIAA increase. Serotonin uptake in vitro in brain slices was temperature-dependent and substrate dependence was such that high-affinity as well as low-affinity systems were indicated. Chlorimipramine inhibited the high-affinity system more effectively than the low-affinity system. LSD inhibited 5-HT accumulation at 0 C but not at 37 C. Preliminary results suggest that LSD-serotonin interaction may involve neuronal and subneuronal -membrane binding sites. Stereospecific binding of-LSD in rat brain synaptosome suspensions appears to be temperature- and concentration-dependent. Stereospecific binding of 3H - LSD is decreased by pretreatment with unlabeled LSD in vivo. Simple indoles such as serotonin, psilocin, psilocybin, bufoteni' decrease the binding by 15-20%, tricyclics such as chlorpromazine decrease it by 40-50% an exception being methiothepin which reduced it to 15-20%. LSD-like derivatives or congeners (BOL, MBL, MLD) almost entirely block the binding. The relation of LSD action to serotoninergic neurons was studied by raphe stimulation in vivo. Raphe neurons were stimulated for 60 min after which LSD was administered and brains removed 60 min later. Results indicated that stimulation of raphe neurons abolished the effect of LSD on 5-HT. In other studies, it was shown that pain increased levels of aspartate and glutamate in subcortical areas, while morphine decreased these levels. Chlorpromazine was half as effective as - morphine in relieving pain in cats. There were 2 types of tolerance to the analgesic effects of morphine; one form is induced by inter-action between morphine and the test procedure while the other develops independently of this interaction. The analgesic response seemed to increase with increasing age of the animal. In the spinal trigeminal tract, phenobarbital and chlorpromazine depress-ed responses induced by gingival and tooth pulp stimulation, and phenobarbital also inhibited responses from the central segmental fasciculus. Responses in the dorsal tegmentum were depressed by morphine.
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