Stimulation of the medullary A1 noradrenergic system augments luteinizing hormone release induced by medial preoptic nucleus stimulation. Evaluation of A1 projections to the hypothalamus and of drugs which affect norepinephrine synthesis and adrenoceptors.

Abstract

Previous reports suggest that A1 noradrenergic projections to the hypothalamus may have stimulatory or inhibitory effects on the release of luteinizing hormone releasing hormone (LH-RH), depending upon the steroid environment of the rat. In the present study, we reevaluated the effects of electrical stimulation (ES) of the A1 cell group on LH release in estrogen-primed, ovariectomized rats which had been anesthetized with chloral hydrate. This anesthetic blocked spontaneous LH surges which normally occur in estrogen-treated ovariectomized rats. ES of the A1 cell group in chloral hydrate treated rats failed to alter basal LH concentrations. Therefore, we evaluate the effects of A1-ES on LH release in rats in which prior electrochemical stimulation (ECS) of the medial preoptic nucleus (MPN) was performed. Bilateral MPN-ECS induced a significant increase in plasma LH. When the A1 cell group was unilaterally stimulated (1 mA) for 15 min, beginning 30 min after MPN-ECS, peak LH concentrations were significantly augmented with peak values being reached at 60 min. Thereafter, plasma LH declined from 75 to 180 min towards basal levels. In a second experiment, unilateral MPN-ECS was performed, and 30 min later either the ipsilateral or contralateral A1 cell group was ES. When MPN + A1 were stimulated on the ipsilateral side of the brain, no amplification in LH release occurred above that obtained after only MPN-ECS. In contrast, contralateral A1-ES markedly amplified LH release, suggesting that most stimulatory A1 fibers decussate to reach contralateral LH-RH neurons.(ABSTRACT TRUNCATED AT 250 WORDS)