Johnston C A, Fagin K D, Alper R H, Negro-Vilar A
Endocrinology. 1986 Feb;118(2):805-10. doi: 10.1210/endo-118-2-805.
The present study was designed to evaluate the role of the neurointermediate pituitary lobe (NIL) in the 5-hydroxytryptophan (5-HTP)-induced increase in plasma PRL levels. The neurochemical mechanisms involved in this neuroendocrine regulation were also analyzed by examining the concentrations of serotonin (5-HT), norepinephrine, and dopamine as well as their primary metabolites in the median eminence (ME), NIL, and anterior pituitary (AP) after different treatments. Removal of the NIL (NIL-X) did not significantly affect basal plasma PRL concentrations or amine metabolism in the ME or AP. 5-HTP administration resulted in a 5-fold increase in plasma PRL in sham-operated (SHAM) animals, but NIL-X completely abolished this PRL response. 5-HTP injection elicited large increases in 5-HT and 5-hydroxyindole-3-acetic acid concentrations in ME, NIL, and AP in SHAM animals, and similar changes within the ME and AP in NIL-X animals, but did not significantly affect norepinephrine or dopamine metabolism in the ME, NIL, or AP of NIL-X or SHAM animals. Moreover, tissue concentrations of 5-HTP after 5-HTP injection increased similarly in SHAM and NIL-X animals. Inhibition of peripheral decarboxylase activity with MK486 prevented the 5-HTP-induced increase in PRL in SHAM animals and the increase in 5-HT metabolism in both SHAM and NIL-X groups. These data indicate that an intact NIL is required for the 5-HTP-induced increase in plasma PRL, but does not seem to be essential for the regulation of basal PRL release. They also demonstrate that the 5-HTP-induced activation of 5-HT metabolism in both ME and AP is not sufficient, by itself, to enhance PRL release.