The probable role of histamine in the rostral hypothalamus on the prolactin and luteinizing hormone release induced by estrogen in conscious spayed rats.

Abstract

The participation of histamine (HA) sensitive sites in the preoptic-anterior hypothalamic area (POA-AHA) on prolactin (PRL) and luteinizing hormone (LH) surge induced by estrogen was studied in ovariectomized rats. Different groups of animals were subjected to the following experimental schedule: On day "0" rats were stereotaxically implanted into the POA-AHA with microinjection cannulae. On day "1", rats were injected s.c. with estrogen. On days "2" and "3", animals were microinjected into the POA-AHA with different drugs, according to the type of experiment, and at day "4", through a silastic cannula implanted previously in the jugular vein, blood samples were taken each hour between 15:00-21:00 h. In the plasma, PRL and LH concentrations were measured by RIA. Four experiments were performed. In Experiment 1, animals at 12:00 h were injected into the POA-AHA with pyrilamine maleate (an H 1-histamine antagonist), metiamide (an H2-histamine antagonist) or saline as control. In Experiment 2, rats at 12:00 h were injected into the POA-AHA with alpha-fluormethyl-histidine (an inhibitor of histamine synthesis) or the combined administration of pyrilamine and metiamide. In Experiment 3, rats previously microinjected with the histamine synthesis inhibitor were microinjected with 4-methyl-histamine (an H 2-histamine agonists) or 2-pyridilethyl-amine (an H 1-histamine agonist) and in Experiment 4, rats were microinjected at 09:00 h with metiamide, pyrilamine, fluor-methyl-histidine or saline as control. Results showed that in animals treated with pyrilamine or metiamide at noon the prolactin surge induced by estrogen was affected (inhibited by metiamide and shortened by pyrilamine, Experiment 1) and LH surge slightly affected. Rats that received FMH or the combined administration of the histamine antagonists the prolactin and LH surge were abolished (Experiment 2). Only the treatment of the H 2-histamine agonist was able to reproduce the prolactin increase in rats treated with FMH. Nor the H 1 or H 2-histamine agonists were effective in reproducing the LH surge in these animals (Experiment 3). Animals that received saline at 09:00 h into the POA-AHA, the prolactin and LH surges were abolished. Results confirm that histamine in the POA-AHA is important for the expression of prolactin and LH surge induced by estrogen and suggest that H 1- and H 2-histamine receptors are involved in the complex timing mechanisms of the rostral hypothalamus that control both hormone release in rats.