Characteristics of prolactin-releasing response to salsolinol (SAL) and thyrotropin-releasing hormone (TRH) in ruminants.

The secretion of prolactin (PRL) is stimulated by thyrotropin-releasing hormone (TRH), and inhibited by dopamine (DA). However, we have recently demonstrated that salsolinol (SAL), a DA-derived endogenous compound, is able to stimulate the release of PRL in ruminants. The aims of the present study were to compare the characteristics of the PRL-releasing response to SAL and TRH, and examine the relation between the effects that SAL and DA exert on the secretion of PRL in ruminants in vivo and in vitro. Three consecutive intravenous (i.v.) injections of SAL (5mg/kg body weight (b.w.): 19.2micromol/kgb.w.) or TRH (1microg/kgb.w.: 2.8nmol/kgb.w.) at 2-h intervals increased plasma PRL levels after each injection in goats (P<0.05); however, the responses to SAL were different from those to TRH. There were no significant differences in each peak value between the groups. The rate of decrease in PRL levels following the peak was attenuated in SAL-treated compare to TRH-treated animals (P<0.05). PRL-releasing responses to SAL were similar to those to sulpiride (a DA receptor antagonist, 0.1mg/kgb.w.: 293.3nmol/kgb.w.). In cultured bovine anterior pituitary (AP) cells, TRH (10(-8)M) significantly increased the release of PRL following both 15- and 30-min incubation periods (P<0.05), but SAL (10(-6)M) did not increase the release during the same periods. DA (10(-6)M) completely blocked the TRH-induced release of PRL for a 2-h incubation period in the AP cells (P<0.05). Sulpiride (10(-6)M) reversed this inhibitory effect but SAL (10(-6)M) did not have any influence on the action of DA. These results show that the mechanism(s) by which SAL releases PRL is different from the mechanism of action of TRH. Furthermore, they also show that the secretion of PRL is under the inhibitory control of DA, and SAL does not antagonize the DA receptor's action.