PITUITARY-DEPENDENT HORMONAL-REGULATION OF GALANINERGIC NEURONS IN THE RAT HYPOTHALAMUS

To investigate whether pituitary-dependent hormones may regulate galan in (GAL) content, synthesis and distribution in the hypothalamus, fema le hypophysectomized Wistar rats were treated for 2 weeks with subcuta neous injections of thyroxine (T-4, 2 x 1 mu g), bovine growth hormone (GH, 2 x 125 mu g), cortisol (C, 50 mu g), subcutaneous implants of b eta-estradiol(E(2), 5-mm implant, dilution 1:1), or with the combinati ons [T-4+GH], [T-4+GH+C+E(2)] or [T-4+GH+C+E(2) + rat PRL, 2 x 125 mu g] doses/100 g BW/day). Concentrations of GAL in the hypothalamus were measured by radioimmunoassay (RIA) and GAL mRNA abundance was quantif ied by Northern blot (6 rats/group); 2 rats/group were used for immuno histochemistry. Hypophysectomy caused decreases of hypothalamic GAL pe ptide and mRNA concentrations (by 70 and 50%, respectively; p < 0.05 v s. intact rats). GAL immunoreactivity disappeared in the median eminen ce (ME), but increased in the neurohypophyseal magnocellular neurons o f hypophysectomized rats. Substitution with T-4, GH, [T-4+GH], C or E( 2) had no significant effect on total hypothalamic GAL peptide and GAL mRNA concentrations. A treatment combining [T-4+GH+C+E(2)] increased hypothalamic GAL (1.9 +/- 0.1 vs. 1.2 +/- 0.1 ng/mg protein in untreat ed hypophysectomized rats; p < 0.01) and GAL mRNA concentrations (127 +/- 19 vs. 59 +/- 2 densitometric units in untreated rats, p < 0.001). Addition of PRL to this combined treatment had no further effect. Tre atment with T-4, GH, [T-4+GH] or E(2) enhanced GAL labeling in the ME of hypophysectomized rats. The effect of estrogens was restricted to t he GnRH-rich lateral regions of the ME. The combined treatment with [T -4+GH+C+E(2)] restored the ME GAL immunoreactivity to levels observed in intact rats. In contrast, the increased GAL labeling observed in ma gnocellular neurons after hypophysectomy was not influenced by any hor monal treatment. In conclusion, hypophysectomy leads to marked reducti ons of hypothalamic GAL and GAL mRNA concentrations, and of GAL immuno reactivity in the ME. These reductions are prevented in part by a comb ined hormonal treatment associating T-4, GH, C and E(2), but not by an y hormone given alone. This suggests specific pituitary hormone-depend ent regulation of the hypophysiotropic GAL neurons. In contrast, the i ncreased GAL labeling in magnocellular neurons of hypophysectomized ra ts persists despite hormonal treatment and likely represents a lesiona l effect on the neurohypophyseal GAL system.