Evidence for the Involvement of Central Epinephrine Systems in the Regulation of Luteinizing Hormone, Prolactin, and Growth Hormone Release in Female Rats*

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Abstract
It has been shown that the stimulatory feedback effects of ovarian hormones on LH release in ovariectomized rats can be blocked by selective inhibition of epinephrine (EPI) synthesis. The purpose of these experiments was to characterize further the role of central and/or peripheral EPI systems in the neural regulation of LH, GH, and PRL secretion in the female rat. Ovariectomized rats were treated with either oil vehicle or a sequential, stimulatory estradiol plus progesterone regimen. Animals in each condition were pretreated with saline vehicle, centrally active EPI synthesis inhibitors (SK & F 64139 or SK & F83593), or SK & F 29661, an EPI synthesis inhibitor that does not cross the blood-brain barrier. The centrally active EPI antagonists blocked the surge of LH, but not the increase in PRL, that occurred after estrogen plus progesterone treatment. These drugs also decreased hypothalamic concentrations of EPI without affecting the other catecholamines. The peripherally active SK & F 29661 did not prevent either LH or PRL surges and did not affect hypothalamic catecholamines. None of the compounds affected LH or PRL concentrations in oil-treated, ovariectomized rats. Neither SK & F 64139 nor SK & F 29661 altered the pulsatile release of LH in ovariectomized, hormonally untreated rats, but SK & F 64139 completely blocked the episodic secretion of GH. The release of LH in response to iv LHRH was minimally affected after EPI synthesis inhibition. SK & F 64139 did not prevent the afternoon rise in PRL induced by estradiol. These experiments indicate that 1) central EPI systems may mediate the positive feedback actions of ovarian hormones on LH secretion, but not the estrogen-induced increase in PRL secretion; 2) central adrenergic systems are involved in the regulation of episodic GH secretion; and 3) central EPI systems do not appear to be involved in the neural regulation of pulsatile LH secretion.

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