α₁-Noradrenergic regulation of hypothalamic progestin receptors and guinea pig lordosis behavior

Experiments were conducted to determine whether α₁- or α₂-receptors mediate noradrenergic (NA) regulation of guinea pig lordosis behavior and hypothalamic progestin receptors. When infused into a lateral cerebroventricle at a dose that inhibits lordosis and that decreases the concentration of estradiol-inducible hypothalamic progestin receptors, phenoxybenzamine decreased binding of the α₁-ligand [³H]WB4101 but not the α₂-ligand [³H]clonidine to brain membranes. Thus, under the conditions used, phenoxybenzamine appears to block α₁-receptors with little or no effect on α₂-receptors. Experiments with the selective α₁-antagonist prazosin also indicated α₁-receptor reguilation of lordosis and hypothalamic progestin receptors. Prazosin inhibited lordosis induced by estradiol benzoate (EB) plus progesterone and by EB + clonidine and decreased the concentration of cytoplamic progrestin receptors in hypothalamus (but not in area or frontal cortex) of EB-primed females. The inhibition of lordosis is apparently not due to some unknown side effect of prazosin because pretreatment with a high dose of clonidine attenuated the inhibition. The possibility that a causal relationship exists between effects of α₁-NA transmission on hypothalamic progestin receptors and lordosis was discussed. Also, because effects of NA transmission on hypothalamic progestin receptors are dependent on prior treatment with EB, it was suggested that NA transmission might influence estradiol action in addition to progestin action in hypothalamic cells.