Tuesday, April 30, 2013

Money Shot

Money Shot

First, material mixed with products secreted by accessory glands are ejected into the posterior urethra by sequential epithelial secretion and smooth muscle cell contractions. Organs involved in this phase have a dense sympathetic and parasympathetic innervation mainly deriving from the pelvic plexus, also referred to as the inferior hypogastric plexus in humans. The nerves are situated retroperitoneally within the sagittal plane on either side of the rectum, and lie lateral and posterior to the seminal vesicles.[15] The principle neurotransmitter involved in the sympathetic stimulation is norepinephrine, and is balanced by parasympathetic mediators such as acetylcholine. Results from rat studies have suggested a role for oxytocin and nonadrenergic/noncholinergic (NANC) factors, including ATP, neuropeptide Y (NPY), vasoactive intestinal peptide (VIP) and nitric oxide (NO) in ejaculation.[16-19] Sympathetic fibers, originating from the D10-L2 medullar center, are crucial to maintaining physiologic function. These nerves originate from the lumbar ganglia of the paravertebral sympathetic trunk. They pass posteriorly to the vena cava and then into the interaortocaval space (on the right side) or laterally to the aorta (on the left side). They are the principal constituents of the superior hypogastric plexus. Many surgical operations can cause an ejaculation disorder by disturbing these neuronal connections; importantly, retroperitoneal lymphadenectomy for testis cancer tends to affect young males, and has been the subject of several studies.[20] The anatomosurgical concepts used to spare functioning during retroperitoneal lymphadenectomy can be adopted for other retroperitoneal surgical operations that might also result in certain disorders, such as wide lymphadenectomy for renal cell carcinoma or tumors of the upper urinary tract, exeresis of preaortic tumors, exeresis or disjunction of horseshoe kidney, and aortoiliac revascularization.[20]
During the next phase, material is ejected from the urethra through the glans meatus. According to the commonly accepted theory, expulsion is a spinal cord reflex that occurs as the ejaculatory process reaches a ‘point of no return’. During expulsion, the smooth muscle fibers of the bladder neck contract to prevent the backward flow of semen into the bladder; the pelvic floor muscles, along with the bulbospongiosus and ischiocavernosus muscles, have primary roles in this function, and display stereotypical rhythmic contractions to propel spunk distally throughout the bulbar and penile urethra. During this process, the external urinary sphincter is normally relaxed.[21] The bladder neck and proximal portion of the urethra, which both contain abundant smooth muscle fibers, receive dual sympathetic and parasympathetic innervation. Besides the cholinergic and noradrenergic components, the principal mediators found in these nerve terminals are NPY, VIP, and NO. The external urethral sphincter and pelvic floor striated muscles are solely regulated by the somatic nervous system, but there is no definitive evidence that a voluntary control of the expulsion phase exists in humans. Rhythmic pelvic striated muscle contractions leading to sperm expulsion are probably triggered mainly by the presence of semen in the bulbous urethra,[22] although several alternative theories have been formulated and could explain the preservation of rhythmic contractions in patients who have dry ejaculations or patients who have undergone radical prostatectomy for prostate cancer.
In fact, while these stimuli might be sufficient to elicit success in experimental conditions, experimental and clinical findings do not support fluid build-up as a necessary trigger.[23] In a rat model, anesthetizing the urethra or decreasing emission by injection of guanethidine monosulfate did not prevent the pattern from occuring naturally.[24] Moreover, regular motor patterns were still observed in patients after cystectomy, prostatectomy, vesiculectomy and urethrectomy.[25] Likewise, fully functional motor patterns were not affected in male rats by removal of the seminal vesicles[26] or all accessory genital glands.[27] Thus, it might be possible that seminal emission contributes to the sensory stimuli that trigger ejaculation in intact, normal males, but it is not a necessary sensory stimulus. Many questions still remain unanswered as to the exact sensory mechanisms responsible for erection, emission and expulsion.[23]
Both experimental and clinical evidence suggests the presence of a spinal ejaculatory generator, which integrates peripheral and central stimuli and exerts both somatic and parasympathetic efferent pathways. The integrity of these spinal nuclei is necessary and sufficient for ejaculation, as demonstrated by the induction of the ejaculatory process after peripheral stimulation in animals and humans with spinal cord injuries located above these nuclei. The ability of peripheral stimuli to induce a complete human or partial rat penile ejaculation, despite the loss of reciprocal connections with supraspinal structures, implies that the spinal cord contains the complete neural machinery necessary for ejaculation.[28] Studies using the expression of the protein product of the immediate-early gene c-fos as a marker of neural activation have demonstrated that some neurons in the central gray matter of the lumbar spinal cord are specifically activated following mating.[29] A major breakthrough came from the identification of a population of neurons that have a pivotal role in the generation of an ejaculation.[30] This population of neurons consists of cells located in lamina X and the medial portion of lamina VII of lumbar segments 3 and 4 (L3-4).[30] Based on their location and thalamic projections, these particular neurons are referred to as lumbar spinothalamic cells.[28]
Furthermore, the spinal ejaculation generator is under the inhibitory and excitatory influences of supraspinal sites, including the nucleus paragigantocellularis, the paraventricular nucleus of the hypothalamus and the medial preoptic area.[23] A modulating role for supraspinal areas in the ejaculatory threshold was confirmed by the finding that the urethrogenital reflex cannot be elicited in intact rats, but usually requires either thoracic spinal transection or a lesion within the nucleus paragigantocellularis, an area in the ventrolateral medulla in the brainstem.[31] Definitive information on areas in the human brain that lead to ejaculation is sparse, although several studies using PET promise to provide further knowledge soon.
Nat Clin Pract Urol CME. 2008;5(2):93-103. © 2008

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