Diurnal rhythmicity of beta-1- and beta-2-adrenergic receptors in ovariectomized, ovariectomized estradiol-treated and proestrous rats

The effect of norepinephrine on LH is complex: the ovarian steroidal milieu appears to determine whether norepinephrine stimulates or inhibits LH secretion. It has been proposed that steroids allow norepinephrine lo have opposite effects on LH by altering the relative concentrations of α₁ stimulatory) and β (inhibitory) adrenergic receptors in the hypothalamus. Thus, many investigators have argued that estradiol may permit norepinephrine to stimulate LH release by increasing the density of α1-and decreasing the density of β-adrenergic receptors in one or more key hypothalamic regions. To test this hypothesis specifically, we measured the density of β₁-and β₂-adrenergic receptor densities in proestrous, ovariectomized, and ovariectomized estradiol-treated rats at various times of day to determine (1) whether the densities or β-receptors exhibit diurnal rhythmicity, (2) whether β-receptors decrease during the time of increased LH secretion and/or (3) how steroidal milieu influences the density and/or the rhythm of receptor densities. The densities of β₁-and β₂-receptors exhibit a diurnal rhythm in some brain areas. These rhythms are detectable only in proestrous and ovariectomized rats and only in selected brain regions. Estrogen treatment has opposing effects in different brain regions. It suppresses the rhythm of β₁-receptor concentrations in ovariectomized rats and also suppresses the average density of receptors in the supra chiasmatic nucleus and pineal gland. In contrast, estrogen increases the density of β₁-re-ceptors in the medial preoptic nucleus. In summary, the results of this study demonstrate that the diurnal rhythm in β-receptors and the effect of estradiol correlate with previously reported changes in receptor-mediated functions. In addition, they reveal the complex interactions of time of day and steroidal milieu on the density of β₁-andβ₂-receptors in various brain regions. Finally, the data strongly suggest that decreases in the densities of β-receptors cannot explain the timing of the proestrous or estradiol-in-duced LH surge or the ability of norepinephrine lo inhibit LH release in ovariectomized rats or stimulate LH release in steroid-treated rats.