The possible participation of the central noradrenergic system in the expression of the ejaculatory reflex of the rat was explored by evaluating the effects of the alpha(2)-adrenoceptor antagonist, yohimbine, on the exhausted coital reflex model. Male sexually experienced Wistar rats, subjected to the coital reflex exhaustion paradigm received a single i.v. injection of yohimbine (10 mug/animal), immediately after reaching exhaustion. Enhancement of noradrenergic transmission by yohimbine provoked the immediate expression of a single ejaculatory genital motor pattern (GMP) similar to a first reflexively evoked one, but in the absence of urethral mechanical stimulation. Pre-treatment with clonidine (10 mug/animal) completely prevented the yohimbine-induced GMP, implying that its effect was exerted upon alpha(2)-adrenoceptors. Clonidine treatment per se induced the expression of a single GMP, similar to a last reflexively evoked one, that was completely blocked by pre-treatment with prazosin (1 mug/animal) indicating that it was due to the a, properties of clonidine. Administration of prazosin previous to yohimbine did not interfere with the expression of the GMP but attenuated it, suggesting the involvement of alpha(1)-adrenoceptors in the yohimbine-induced motor response. Data reveal a facilitatory influence of the noradrenergic system on ejaculatory function mediated by both alpha(1)- and alpha(2)-adrenoceptors and support the notion of yohimbine acting at a spinal level. (C) 2002 Elsevier Science B.V. All rights reserved.