Previous reports suggest that Al 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 Al 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 Al cell group in chloral hydrate treated rats failed to alter basal LH concentrations. Therefore, we evaluated the effects of Al-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 Al 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 Al 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 Al-ES markedly amplified LH release, suggesting that most stimulatory Al fibers decussate to reach contralateral LH-RH neurons. Moreover, in rats which received contralateral MPN + A1 stimulation (0.1 mA), plasma LH reached peak concentrations and then remained significantly higher than in controls (MPN-ECS group) throughout the rest of the experiment. In the third experiment, we evaluated the effects of drugs which affect norepinephrine synthesis or are antagonists of beta or alpha adrenoreceptors. Diethyldithiocarbamate, a dopamine-β-hydroxylase inhibitor, and phenoxybenzamine, an alpha adrenoreceptor antagonist, completely blocked Al-ES-induced amplification of LH release. Propranolol, a beta adrenoreceptor antagonist, did not suppress the effects of Al stimulation on LH secretion. None of these drugs had any appreciable effect on the patterns or concentrations of LH which were released by MPN-ECS. We conclude that LH release can be amplified following Al-ES, but only after preliminary depolarization of LH-RH neurons. We also provide evidence that the major stimulatory Al projections decussate to enter contralateral hypothalamic regions which contain LH-RH neurons. Finally, our pharmacological data suggest that the principal neurotransmitter involved in amplifying LH release may be either norepinephrine or epinephrine as an alpha but not a beta adrenoreceptor antagonist completely blocks the response of LH-RH neurons to Al-ES