Abstract
The change in forebrain 5‐hydroxyindoleacetic acid (5‐HIAA) concentration induced by raphe stimulation has been studied in rats treated with Li+ or 0.9% w/v NaCl solution (saline) for 10 days. Raphe stimulation increased the forebrain concentration of 5‐HIAA in both groups of animals. Chlorimipramine abolished this effect in the control group, but not in the Li+ group. The inhibition of 5‐hydroxytryptamine (5‐HT) uptake by chlorimipramine was not affected by pretreatment with Li+ or by the addition of Li+ to synaptosomal suspensions in vitro. It is suggested that the production of 5‐HIAA following raphe stimulation in Li+‐treated animals is derived from the metabolism of 5‐HT which remains within the intracellular environment. The consequence of this in relation to transmitter release is discussed.