The succession of erection, emission, ejaculation, and orgasm creates the impression that these events might have a common physiologic substrate. In reality, they are separate events. This separateness is clearly illustrated by the typical patient with male orgasmic disorder (MOD), who complains of sustaining hard erections without being able to ejaculate, or by the typical patient with erectile dysfunction, who complains of ejaculating through a flaccid penis.
Emission and ejaculation usually require external genital stimulation (nocturnal emission being the notable exception). Afferent impulses travel through the dorsal nerve of the penis, which is the deepest division of the pudendal nerves, to the S2-S4 dorsal root ganglia. Parasympathetic innervation to the penis originates from the intermediolateral columns of the S2-S4 sacral spinal segments. Sympathetic fibers from the T-11 to L-2 spinal segments travel through via the hypogastric plexus. The efferent impulses activate secretions and transport sperm from the distal epididymis, vasa deferentia, seminal vesicles, and prostate to the prostatic urethra. Closure of the internal urethral sphincter and concomitant relaxation of the external sphincter direct semen into the bulbous urethra, resulting in emission.
The somatomotor efferent of the pudendal nerve then produces subsequent rhythmic contractions of the bulbocavernous muscle, forcing the semen through a pressurized passage (the narrowed urethral lumen compressed by the engorged corpora cavernosa) and yielding 2–5 mL of ejaculate. Because this action is involuntary, integrated autonomic and somatic actions are required for completion.
The cerebral network modulating and controlling the final common output from all ejaculatory stimuli includes the posteromedial bed nucleus of the stria terminalis, the posterodorsal medial amygdaloid nucleus, the posterodorsal preoptic nucleus, and the parvicellular part of the subparafascicular thalamus. [6]
It has been suggested that the ejaculatory reflex is primarily regulated by the central serotonergic and dopaminergic systems, [7] with other neurotransmitters (eg, acetylcholine, adrenaline, neuropeptides, oxytocin, gamma-aminobutyric acid [GABA], and nitric oxide) playing important roles. [8]
Experimental evidence indicates that serotonin (5-HT), throughout brain descending pathways, exerts an inhibitory role on ejaculation. To date, 3 serotonin receptor subtypes (5-HT1A, 5-HT1B, and 5-HT2C) have been postulated to mediate the modulating activity of serotonin on ejaculation. Pharmacologic manipulation of the serotonergic system has been performed in rats, with the selective serotonin reuptake inhibitors (SSRIs) exhibiting the greatest efficacy in delaying ejaculation. [9]
It has been suggested that the presynaptic 5-HT1A somatodendritic autoreceptors, located in the mesencephalic and medullary raphe nuclei and responsible for decreasing 5-HT release into the synapse, decrease ejaculatory latency. In contrast, the postsynaptic 5-HT1B and 5-HT2C receptors have been shown to prolong ejaculatory latency. [9]
In view of the relation between the serotonergic receptors and their inhibitory and excitatory effects, it is likely that altered levels of 5-HT or altered 5-HT receptor sensitivity in the ejaculatory modulating centers of the central nervous system (CNS) contribute to the pathophysiologic mechanism behind ejaculatory disorders. Thus, 5-HT might suppress ejaculation by interrupting the action of oxytocin, which normally accompanies sexual behavior. [10]
Dopamine plays an important role in the male sexual response. [11] In animal models, dopamine levels in the medial preoptic area of the hypothalamus were shown to increase progressively during excitation and intercourse, [7] GABA-receptor antagonists were found to inhibit sexual behavior, and muscular contractions during ejaculation appeared to be mediated by oxytocin. [8]
Despite significant advances, the specific role and importance of each individual neurotransmitter in the multifactorial and complex ejaculatory reflex remain to be clarified. [12] Research into these subjects is ongoing.
The mechanism of orgasm is still the least well understood part of the sexual process. It probably involves central (cerebral) integration and response to sexual stimulation. Emission, ejaculation, and orgasm are typically associated with several other concomitant nongenital responses, which may include involuntary rhythmic contractions of the anal sphincter, hyperventilation, tachycardia, and elevation of blood pressure.
Transient sympathoadrenal activation during sexual activity, reflected by increases in epinephrine and norepinephrine plasma levels, together with increased cardiovascular activity, has been reported to be associated with orgasm in males.
The association of vasopressin, cortisol, luteinizing hormone (LH), follicle-stimulating hormone (FSH), growth hormone (GH), beta-endorphin, and testosterone with male orgasm remains unclear. Whereas both oxytocin and prolactin levels have been reported to peak immediately after orgasm, plasma prolactin levels seem to represent a more sustained and reliable endocrine marker of orgasm in males. [13, 14]
