Serotonin and Alcohol Consumption

Abstract

Overwhelming experimental evidence suggests that treatments which increase 5-HT availability in the CNS reduce ethanol consumption. For instance 5-HT precursors i.e tryptophan, 5-hydroxytryptophan (Zabik et al, 1985), 5-HT agonists e.g quipazine (Zabik et al, 1985), MK212 (Lawrin et al, 1986), intra-cerebrally-administered 5-HT (Hill, 1974), and selective 5-HT reuptake inhibitors e.g fluoxetine (Murphy et al, 1988; Haraguchi et al, 1990), zimelidine (Amit et al, 1984) all reduce alcohol intake in free choice paradigms. However these same treatments similarly effect food consumption (see Table 1 for summary). Interestingly, the effect of reducing central 5-HT tone fails to consistently elevate ethanol and food intake (see Table 1 for summary). This may imply that a low endogenous 5-HT tone is a prerequisite for ethanol consumption—a hypothesis supported by the fact that genetically derived rat strains which consume large quantities of ethanol show comparatively low forebrain serotonin function (see McBride et al, 1990; Rezvani et al, 1990).