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自发性高血压大鼠中与排尿通路相关的传出和传入神经元肥大。

Efferent and afferent neuronal hypertrophy associated with micturition pathways in spontaneously hypertensive rats.

作者信息

Clemow D B, McCarty R, Steers W D, Tuttle J B

机构信息

Department of Neuroscience, University of Virginia School of Medicine, Charlottesville 22908, USA.

出版信息

Neurourol Urodyn. 1997;16(4):293-303. doi: 10.1002/(sici)1520-6777(1997)16:4<293::aid-nau5>3.0.co;2-9.

Abstract

Elevated nerve growth factor secreted by bladder smooth muscle may be associated with noradrenergic hyperinnervation of the bladder and hyperactive voiding in spontaneously hypertensive rats (SHR) and rats with bladder outlet obstruction. The present study was undertaken to determine if changes occur in efferent and afferent pathways supplying the SHR bladder similar to those in rats with bladder outlet obstruction. Fluoro-Gold (FG) retrograde tracing studies were conducted to examine the postganglionic efferent limb (major pelvic ganglion; MPG) and sensory afferent limb (L1, L2, L6, and S1 dorsal root ganglion; DRG) of the micturition reflex pathway of the SHR and Wistar-Kyoto (WKY) normotensive rat. A significant increase in cross sectional area profiles for labeled neurons in the MPG was observed in SHRs (830.5 +/- 9.0 microns2) as compared to WKYs (736.3 +/- 16.6 microns2). Neuronal cell areas in L2 (1,010.9 +/- 18.6 microns2) and S1 (1,024.6 +/- 28.3 microns2) of SHRs were significantly larger than those of WKYs (L2, 865.3 +/- 12.6 microns2, S1, 778.3 +/- 11.2 microns2). There was an increase in number of labeled cells in L6 within SHRs over WKYs. These results provide evidence that both efferent and afferent changes in neuronal innervation of the bladder occur in SHRs. The SHR strain may represent a genetic model to study changes in micturition reflex pathways that result from alterations in neuronal morphology such as those that occur with urethral outlet obstruction.

摘要

膀胱平滑肌分泌的神经生长因子升高可能与自发性高血压大鼠(SHR)及膀胱出口梗阻大鼠的膀胱去甲肾上腺素能神经超支配和排尿亢进有关。本研究旨在确定供应SHR膀胱的传出和传入通路是否发生与膀胱出口梗阻大鼠类似的变化。采用荧光金(FG)逆行追踪研究来检查SHR和Wistar-Kyoto(WKY)正常血压大鼠排尿反射通路的节后传出支(主要盆神经节;MPG)和感觉传入支(L1、L2、L6和S1背根神经节;DRG)。与WKY大鼠(736.3±16.6平方微米)相比,SHR大鼠(830.5±9.0平方微米)MPG中标记神经元的横截面积显著增加。SHR大鼠L2(1,010.9±18.6平方微米)和S1(1,024.6±28.3平方微米)的神经元细胞面积显著大于WKY大鼠(L2,865.3±12.6平方微米,S1,778.3±11.2平方微米)。与WKY大鼠相比,SHR大鼠L6中标记细胞数量增加。这些结果证明SHR大鼠膀胱神经支配的传出和传入均发生了变化。SHR品系可能代表一种遗传模型,用于研究由神经元形态改变(如尿道出口梗阻时发生的改变)导致的排尿反射通路变化。

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