Estradiol regulates the number of ?(1) but not ? or ?(2) noradrenergic receptors in hypothalamus of female rats.
Present experiments examined whether previously observed hormone-dependent differences in norepinephrine-stimulated cAMP accumulation in hypothalamic and preoptic area slices are attributable to differences in noradrenergic receptor number or binding affinity. When compared to ovariectomized controls, hypothalamic and preoptic area membranes from estradiol-treated rats had significantly elevated numbers of [(3)H]prazosin (?(1)) binding sites. Estradiol affected neither the number of ?(1) sites in frontal cortex nor the affinity of [(3)H]prazosin binding in any brain region sampled. Estradiol had no effect on [(3)H]idazoxan (?(2)) or [(3)H]dihydroalprenolol (?) binding in hypothalamus, preoptic area or cortex. Progesterone reversed estradiol elevation of prazosin binding in preoptic area but had no other measurable effects on any noradrenergic receptor binding when given alone or in combination with estradiol. Neither estradiol nor progesterone altered binding of radiolabeled antagonists when they were included in the in vitro incubation mixture. These data suggest that the increased ?(1) receptor augmentation of cAMP accumulation seen in hypothalamic and preoptic area slices from estradiol-treated rats is correlated with increased ?(1) receptor number. In contrast, estradiol attenuation of ? receptor function and progesterone depression of norepinephrine-stimulated cAMP generation in slices from estradiol-treated females is not correlated with downregulation of any noradrenergic receptor subtype.
Etgen
A M
AM
Departments of Psychiatry and Neuroscience, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, U.S.A.
Karkanias
G B
GB