Park Jee Soo, Jin Mei Hua, Hong Chang Hee
Department of Urology, Yonsei University College of Medicine, Seoul, Korea.
Int Neurourol J. 2018 Jun;22(2):90-98. doi: 10.5213/inj.1836124.062. Epub 2018 Jun 30.
The neurological molecular mechanisms underlying the voiding dysfunction associated with nonbacterial chronic prostatitis/chronic pelvic pain syndrome remain poorly understood. In this study, we assessed whether prostate inflammation activated bladder afferent neurons, leading to bladder dysfunction, and sought to elucidate the underlying mechanisms.
Thirty male Sprague-Dawley rats were divided into 3 groups: sham-saline, formalin-injected, and capsaicin-pretreated and formalin-injected. Chemical prostatitis was induced by 0.1 mL of 10% buffered formalin injected into the ventral prostate. Capsaicin was injected subcutaneously to desensitize capsaicin-sensitive nerves. In each group, conscious cystometry was performed, and c-fos expression within the spinal cord was determined immunocytochemically. Double immunofluorescent staining with c-fos and choline acetyltransferase (ChAT) was performed. On the third day after pseudorabies virus (PRV) infection, c-fos and PRV double-staining was performed.
Intraprostatic formalin significantly increased the maximal voiding pressure and decreased the intercontraction interval, compared with controls. Pretreatment with capsaicin significantly reversed these effects. More c-fos-positive cells were observed in the sacral parasympathetic nucleus (SPN) and dorsal gray commissure (DCM) in the prostatitis group than in the sham group. c-fos-positive cells decreased in the capsaicin-pretreated group. Preganglionic neurons labeled by c-fos and ChAT were observed in the SPN in rats with prostatitis. Interneurons labeled by c-fos and PRV were identified in the DCM after PRV infection.
Our results suggest that prostate inflammation activates afferent nerve fibers projecting to the lumbosacral spinal cord, producing reflex activation of spinal neurons innervating the bladder and bladder hyperreflexia. This is mediated by capsaicin-sensitive prostate afferent neurons.
与非细菌性慢性前列腺炎/慢性盆腔疼痛综合征相关的排尿功能障碍的神经分子机制仍知之甚少。在本研究中，我们评估前列腺炎症是否激活膀胱传入神经元，导致膀胱功能障碍，并试图阐明其潜在机制。
将30只雄性Sprague-Dawley大鼠分为3组：假手术-生理盐水组、注射福尔马林组和辣椒素预处理后注射福尔马林组。通过向腹侧前列腺注射0.1 mL 10%的缓冲福尔马林诱导化学性前列腺炎。皮下注射辣椒素使辣椒素敏感神经脱敏。每组均进行清醒膀胱测压，并通过免疫细胞化学法测定脊髓内的c-fos表达。进行c-fos和胆碱乙酰转移酶（ChAT）的双重免疫荧光染色。在伪狂犬病病毒（PRV）感染后第三天，进行c-fos和PRV双重染色。
与对照组相比，前列腺内注射福尔马林显著增加了最大排尿压力并缩短了收缩间隔。辣椒素预处理可显著逆转这些效应。前列腺炎组骶副交感核（SPN）和背侧灰质连合（DCM）中观察到的c-fos阳性细胞比假手术组更多。辣椒素预处理组中c-fos阳性细胞减少。在前列腺炎大鼠的SPN中观察到由c-fos和ChAT标记的节前神经元。PRV感染后，在DCM中鉴定出由c-fos和PRV标记的中间神经元。
我们的结果表明，前列腺炎症激活投射至腰骶脊髓的传入神经纤维，导致支配膀胱的脊髓神经元反射性激活及膀胱反射亢进。这由辣椒素敏感的前列腺传入神经元介导。
