Abstract
Unilateral kainic acid lesion of the rat centromedian-parafascicular complex (CM-PF) of the thalamus induced a decrease in the 5-hydroxyindole acetic acid/5-hydroxytryptamine ratio both in ipsi and contralateral striatum and substantia nigra, and an increase in both ipsi and contralateral frontal cerebral cortex. No change in apparent serotonin turnover was detected in anterior raphe nuclei. Serotonin synthesis, estimated by measuring 5-hydroxytryptophan accumulation after injection of a decarboxylase inhibitor, was not affected by the CM-PF lesion. The possible pathways involved in the control of serotonin transmission by CM-PF are discussed.

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