Abstract:The adult prostate gland grows and develops under hormonal control while its physiological functions are controlled by the autonomic nervous system. The prostate gland receives sympathetic input via the hypogastric nerve and parasympathetic input via the pelvic nerve. In addition, the hypogastric and pelvic nerves also provide sensory inputs to the gland. This review provides a summary of the innervation of the adult prostate gland and describes the changes which occur with age and disease. Growth and developm… Show more
“…The prostate is highly innervated ( 33 ), and the nerves are required for formation of the prostate during embryogenesis, maturation during puberty, and maintenance of the adult phenotype ( 34 ). Thus, like androgen stimulation, sympathetic stimuli contribute to prostatic differentiation in vivo ( 35 ).…”
Section: Adrenergic Receptor’s Functional Role In the Prostatementioning
confidence: 99%
“…In normal prostate physiology, the sympathetic nervous system regulates prostate differentiation and secretory activity of luminal cells, predominantly through ADRB2 ( 34 , 35 , 40 , 41 ). We know from in vitro and in vivo prostate cancer models that chronic elevation of ADRB activity by exposing mice to repeated stress or by adding ADRB agonists promotes neuroendocrine differentiation ( 70 , 84 – 86 ), metastasis ( 58 , 103 ), angiogenesis ( 78 , 81 , 112 , 115 ), and apoptosis-resistance ( 116 , 120 ); together indicating that adrenergic signaling promotes prostate cancer progression (Figure 2 ).…”
Section: Controversies Clinical Implications and Conclusionmentioning
Enhanced sympathetic signaling, often associated with obesity and chronic stress, is increasingly acknowledged as a contributor to cancer aggressiveness. In prostate cancer, intact sympathetic nerves are critical for tumor formation, and sympathectomy induces apoptosis and blocks tumor growth. Perineural invasion, involving enrichment of intra-prostatic nerves, is frequently observed in prostate cancer and is associated with poor prognosis. β2-adrenergic receptor (ADRB2), the most abundant receptor for sympathetic signals in prostate luminal cells, has been shown to regulate trans-differentiation of cancer cells to neuroendocrine-like cells and to affect apoptosis, angiogenesis, epithelial–mesenchymal transition, migration, and metastasis. Epidemiologic studies have shown that use of β-blockers, inhibiting β-adrenergic receptor activity, is associated with reduced prostate cancer-specific mortality. In this review, we aim to present an overview on how β-adrenergic receptor and its downstream signaling cascade influence the development of aggressive prostate cancer, primarily through regulating neuroendocrine differentiation.
“…The prostate is highly innervated ( 33 ), and the nerves are required for formation of the prostate during embryogenesis, maturation during puberty, and maintenance of the adult phenotype ( 34 ). Thus, like androgen stimulation, sympathetic stimuli contribute to prostatic differentiation in vivo ( 35 ).…”
Section: Adrenergic Receptor’s Functional Role In the Prostatementioning
confidence: 99%
“…In normal prostate physiology, the sympathetic nervous system regulates prostate differentiation and secretory activity of luminal cells, predominantly through ADRB2 ( 34 , 35 , 40 , 41 ). We know from in vitro and in vivo prostate cancer models that chronic elevation of ADRB activity by exposing mice to repeated stress or by adding ADRB agonists promotes neuroendocrine differentiation ( 70 , 84 – 86 ), metastasis ( 58 , 103 ), angiogenesis ( 78 , 81 , 112 , 115 ), and apoptosis-resistance ( 116 , 120 ); together indicating that adrenergic signaling promotes prostate cancer progression (Figure 2 ).…”
Section: Controversies Clinical Implications and Conclusionmentioning
Enhanced sympathetic signaling, often associated with obesity and chronic stress, is increasingly acknowledged as a contributor to cancer aggressiveness. In prostate cancer, intact sympathetic nerves are critical for tumor formation, and sympathectomy induces apoptosis and blocks tumor growth. Perineural invasion, involving enrichment of intra-prostatic nerves, is frequently observed in prostate cancer and is associated with poor prognosis. β2-adrenergic receptor (ADRB2), the most abundant receptor for sympathetic signals in prostate luminal cells, has been shown to regulate trans-differentiation of cancer cells to neuroendocrine-like cells and to affect apoptosis, angiogenesis, epithelial–mesenchymal transition, migration, and metastasis. Epidemiologic studies have shown that use of β-blockers, inhibiting β-adrenergic receptor activity, is associated with reduced prostate cancer-specific mortality. In this review, we aim to present an overview on how β-adrenergic receptor and its downstream signaling cascade influence the development of aggressive prostate cancer, primarily through regulating neuroendocrine differentiation.
“…The prostate growth's anatomical obstruction may be the main reason for lower urinary tract symptoms, but inflammation, infection, and metabolic disorders can also be possible etiologies [76]. The prostate is innervated with the parasympathetic and sympathetic nerves [77]. The cholinergic nerves and muscarinic receptors are present in the fibromuscular stroma of the prostate, which can explain the previous beneficial effects of BoNT-A intraprostatic injection treatments [78][79][80][81].…”
Intravesical botulinum toxin (BoNT) injection is effective in reducing urgency and urinary incontinence. It temporarily inhibits the detrusor muscle contraction by blocking the release of acetylcholine (Ach) from the preganglionic and postganglionic nerves in the efferent nerves. BoNT-A also blocks ATP release from purinergic efferent nerves in the detrusor muscle. In afferent nerves, BoNT-A injection markedly reduces the urothelial ATP release and increases nitric oxide (NO) release from the urothelium. BoNT-A injection in the urethra or bladder has been developed in the past few decades as the treatment method for detrusor sphincter dyssyndergia, incontinence due to neurogenic or idiopathic detrusor overactivity, sensory disorders, including bladder hypersensitivity, overactive bladder, and interstitial cystitis/chronic pelvic pain syndrome. Although the FDA only approved BoNT-A injection treatment for neurogenic detrusor overactivity and for refractory overactive bladder, emerging clinical trials have demonstrated the benefits of BoNT-A treatment in functional urological disorders. Cautious selection of patients and urodynamic evaluation for confirmation of diagnosis are crucial to maximize the successful outcomes of BoNT-A treatment.
“…Dense neuropeptide Y innervation is present throughout the prostatic stroma but most studies have not found the neuropeptide to be involved in the contraction of the prostate (White et al, ).…”
Section: Neural Innervation Of the Prostatementioning
confidence: 99%
“…If the pelvic muscles do not contract the semen emission is one of dribbling, powered by the peristaltic contractions of the urethra alone with little ecstatic pleasure (Newman et al, ). Although orgasm normally takes place concomitantly with ejaculation, the two processes are actually independent (Levin, ).While the prostate is involved in forming part of the ejaculate (as detailed above) it is also involved in ejaculation per se as its fibromuscular covering containing smooth muscle contracts clonically under its adrenergic innervation propelling the semen from the prostatic urethra into the penile urethra (White et al, ).…”
Current medical literature does not describe precisely the activation and mechanisms of prostate orgasms. This brief review describes what we know about the anatomy and physiology of the prostate and its involvement in reproduction and especially its stimulation for sexual recreation. It is illustrated with a highly relevant case history. Clin. Anat. 31:81-85,
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