Data issued from morphological and physiological experiments suggests that the noradrenergic system, through ascending pathways to the brain and descending pathways to the spinal cord, may regulate male sexual functions. Adrenoceptors have been shown to be present in the brain and spinal cord of animals and humans. The activity of spinal preganglionic neurons is modulated by noradrenaline. Pharmacological approaches aiming at selectively targeting α1- or α2-adrenoceptors have been conducted in patients with erectile dysfunction or in monkeys and rats in a variety of tests. Briefly, conclusions arising from these studies are: activation of α1-adrenoceptors facilitates copulation, where activation of α2-adrenoceptors inhibits copulation. α2-adrenoceptors antagonists like yohimbine facilitate sexual behavior, reducing ejaculation latency in male rats and increasing their sexual motivation. Furthermore, yohimbine induces copulation in rats either castrated or sexually naive. In contrast, activation of α1-adrenoceptors depresses sexual responses in another context, i.e. reflexive erections. Activation of α2-adrenoceptors activates reflexive erections in rats, and α2-adrenoceptors antagonists (yohimbine) inhibit them. Today’s challenge is to separate the effects of any drug acting at the level of the α-adrenoceptors on the central vs. peripheral control of sexual functions, on the brain vs. spinal cord control of the same functions, and the search for any specialization of α-adrenoceptors subtypes in a given sexual function. Treatment of sexual dysfunctions in man (e.g. ejaculation) focusing on the spinal cord as a pharmacological target should also be expanded. Finally, considering the similarities between neural networks controlling male and female sexual functions, the treatment of female sexual dysfunction with comparable pharmacological approaches should be evaluated.

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