Effects of LSD and BOL on the catecholamine synthesis and turnover in various brain regions.

Abstract

In the rat, lysergic acid diethylamide (LSD) 0.5 mg/kg and 2-bromo lysergic acid diethylamide (BOL) 0.5 mg/kg increased the rate of the striatal in vivo tyrosine hydroxylation as measured by the DOPA accumulation after decarboxylase inhibition. Neither LSD nor BOL significantly changed the DOPA accumulation in the olfactory tubercle, a dopamine-rich part of the limbic system. LSD but not BOL increased the DOPA accumulation in the cerebral cortex and in the brain stem. LSD and BOL appeared not to alter the rate of alpha-MT-induced disappearance of DA or of NA in the whole brain, nor did they change the rate of the alpha-MT-induced disappearance of DA in the striatum. It is suggested that in the striatum LSD and BOL block autoreceptorss (presynaptic receptors) regulating the tyrosine hydroxylation. These receptors may be DA receptor, but may also be 5-HT- or LSD-sensitive receptors. The regional differences observed between LSD and BOL suggest that LSD in the cerebral cortex and in the brain stem increases the DOPA accumulation by mechanism other than that functioning in the striatum. One possible explanation is that LSD and BOL may differ in their effects on 5-hydroxytryptaminergic systems in the cerebral cortex and in the brain stem.