Male sexual responses are reflexes mediated by the spinal cord and modulated by neural circuitries involving both the peripheral
and central nervous system. While the brain interact with the reflexes to allow perception of sexual sensations and to exert excitatory
or inhibitory influences, penile reflexes can occur despite complete transections of the spinal cord, as demonstrated by the reviewed animal
studies on spinalization and human studies on spinal cord injury. Neurophysiological and neuropharmacological substrates of the
male sexual responses will be discussed in this review, starting with the spinal mediation of erection and its underlying mechanism with
nitric oxide (NO), followed by the description of the ejaculation process, its neural mediation and its coordination by the spinal generator
of ejaculation (SGE), followed by the occurrence of climax as a multisegmental sympathetic reflex discharge. Brain modulation of these
reflexes will be discussed through neurophysiological evidence involving structures such as the medial preoptic area of hypothalamus
(MPOA), the paraventricular nucleus (PVN), the periaqueductal gray (PAG), and the nucleus para-gigantocellularis (nPGI), and through
neuropharmacological evidence involving neurotransmitters such as serotonin (5-HT), dopamine and oxytocin. The pharmacological developments
based on these mechanisms to treat male sexual dysfunctions will complete this review, including phosphodiesterase (PDE-5)
inhibitors and intracavernous injections (ICI) for the treatment of erectile dysfunctions (ED), selective serotonin reuptake inhibitor
(SSRI) for the treatment of premature ejaculation, and cholinesterase inhibitors as well as alpha adrenergic drugs for the treatment of anejaculation
and retrograde ejaculation. Evidence from spinal cord injured studies will be highlighted upon each step.
Keywords: Erection, emission, ejaculation, orgasm, spinal generator of ejaculation (SGE), autonomic dysreflexia, spinal cord injury (SCI).
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