The sigma receptor ligand rimcazole alters secretion of prolactin and alpha-melanocyte stimulating hormone by dopaminergic and non-dopaminergic mechanisms.

The role of tuberoinfundibular and periventricular-hypophysial dopaminergic neurons in mediating rimcazole-induced decreases in plasma concentrations of prolactin and alpha-melanocyte stimulating hormone was assessed. Dopaminergic neuronal activity was estimated by measuring concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC) in the median eminence and intermediate lobe of the pituitary which contain terminals of tuberoinfundibular and periventricular-hypophysial dopaminergic neurons, respectively. Rimcazole decreased plasma concentrations of both prolactin and alpha-melanocyte stimulating hormone, increased the concentration of DOPAC in median eminence, but did not alter DOPAC concentrations in the intermediate lobe of the pituitary. Pretreatment with a 'putative' sigma receptor agonist, pentazocine, prevented the rimcazole-induced increase of the concentration of DOPAC in the median eminence, but did not block the ability of rimcazole to decrease plasma concentrations of prolactin. The results of this study reveal that the ability of rimcazole to decrease alpha-melanocyte stimulating hormone secretion is not mediated by a dopaminergic mechanism, whereas the ability of rimcazole to decrease prolactin secretion appears to be mediated by both dopaminergic and non-dopaminergic mechanisms.