Further evidence of noradrenergic regulation of rat hypothalamic estrogen receptor concentration: possible non-functional increase and functional decrease.
The regulation of estrogen receptors by the alpha 2-noradrenergic system was studied. A single injection of the alpha 2-noradrenergic antagonist, yohimbine, caused a biphasic effect on the concentration of cytosol estrogen receptors in the mediobasal hypothalamus and anterior pituitary gland. A short-latency increase was seen at 1.5-3 h, followed by a longer-lasting decrease at 8-16 h. Scatchard analysis revealed that the apparent, short-latency increase is in the concentration of binding sites, not in the affinity of the receptor for [3H]estradiol. The increase in the concentration of cytosol estrogen receptors is not blocked by pretreatment with the alpha 2-noradrenergic agonist, clonidine. In addition, no increase is detected in the concentration of cell nuclear estrogen receptors accumulating in response to a saturating dose of estradiol. Therefore, the apparent increase in the concentration of cytosol estrogen receptors may not represent a functional increase in receptors. The decrease in the concentration of estrogen receptors, which occurs 8-16 h after yohimbine treatment, is also seen after injection of the alpha 2-adrenergic antagonist, idazoxan, and is not due to a change in the in vitro rate of association of the receptors with [3H]estradiol. Furthermore, the decrease seems to be a functional decrease in the concentration of receptors capable of cell nuclear accumulation in response to estradiol injection, as indicated by the results of experiments in which the concentration of cell nuclear estrogen receptors was assayed after estradiol injection. These experiments provide further support for the hypothesis that the alpha-noradrenergic system, and perhaps specifically the alpha 2-subtype, is involved in decreasing the concentration of estrogen receptors in parts of the brain and pituitary gland. This interaction provides a mechanism by which the environment could regulate the sensitivity of certain neurons to estradiol. However, the finding that the initial increase in the concentration of cytosol estrogen receptors after yohimbine treatment is not followed by the predicted increase in cell nuclear estrogen receptors after estradiol injection raises questions about the physiological relevance of the apparent increase under some conditions.
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D003000:Clonidine / Q000494:pharmacology; D003600:Cytosol / Q000502:physiology; D004146:Dioxanes / Q000494:pharmacology; D005260:Female; D007031:Hypothalamus / Q000187:drug effects / Q000502:physiology*; D019329:Idazoxan; D051381:Rats; D011919:Rats, Inbred Strains; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects*; D011960:Receptors, Estrogen / Q000187:drug effects / Q000502:physiology*; D015016:Yohimbine / Q000494:pharmacology*
D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D004146:Dioxanes; D011942:Receptors, Adrenergic, alpha; D011960:Receptors, Estrogen; D015016:Yohimbine; D003000:Clonidine; D019329:Idazoxan