人工反射弧建立后大鼠膀胱胆碱能神经的形态学变化

目的观察体神经一内脏神经人工反射弧建立后,大鼠膀胱肌间神经丛分布的改变以及神经肌肉接头处的变化。方法Sprague—Dawley大鼠随机分为三组：对照组、脊髓横断组和手术重建组。手术重建组大鼠术后饲养3个月,与脊髓横断组大鼠一起进行脊髓横断,再继续饲养3个月,对照组不做任何处理。DiI进行逆行神经追踪;免疫荧光的方法显示DiI阳性标记细胞中的胆碱乙酰转移酶（cholineacetyltransferase,CHAT）;改良的Kamovsky—Roots法检测膀胱铺片中神经纤维的分布。结果DiI阳性标记细胞主要分布于脊髓L3尾部至L5头侧前角,ChAT阳性细胞和DiI阳性标记细胞部分重叠。手术重建组和对照组相比,膀胱肌间神经纤维的数量较少,染色浓度也较浅护〈0．05）;而手术重建组神经纤维密度较脊髓横断组增大,染色浓度增强妒〈0．05）,且出现明显的神经再分布。结论人工体内脏神经反射弧建立后,新的传出支为体神经,可以长入副交感神经纤维,传出神经元的递质仍为乙酰胆碱,膀胱内胆碱能神经纤维再生和乙酰胆碱活性增强且出现神经再分布,这可能在膀胱的控制性排尿中起作用。     

神经生长因子及其结合肌基膜管移植修复脊髓横断性损伤的组织学观察

目的 对应用神经生长因子（ＮＧＦ）及其结合肌基膜管（ＭＢＬ）修复脊髓横断性损伤进行组织学评价。方法 横断雌性家犬脊髓后,分为三组：（Ａ）ＭＢＬ移植结合注射ＮＧＦ组７只。（Ｂ）脊髓单纯横断注射ＮＧＦ组６只。（Ｃ）对照组切除脊髓０．５ｃｍ４只。六个月后用免疫且化学方法对神经轴突和胶质细胞网络框架结构,进行特异染色,并用图像分析方法对脊髓横断处的远近端横截面进行神经纤维数量对比。结果 各组远端神经纤维数     

生物素标记葡聚糖胺神经束路示踪见证神经干细胞移植后皮质脊髓书的再生

实验旨在运用生物素标记葡聚糖胺神经束路示踪标记神经干细胞移植治疗脊髓损伤后皮质脊髓束的再生和神经的重新支配状况,结果表明神经干细胞移植治疗胸10脊髓横断损伤大鼠运动功能评分在横断损伤3周后逐渐升高。治疗后12周有部分生物素标记葡聚糖胺阳性标记的皮质脊髓束再生通过脊髓横断损伤部位,电镜检查发现再生的生物素标记葡聚糖胺阳性标记的神经终末与损伤远端神经元形成新的突触联系。说明生物素标记葡聚糖胺神经束路示踪能有效提供脊髓损伤后神经恢复的解剖形态学依据。     

局部注射骨髓间充质干细胞治疗大鼠脊髓损伤：运动功能有改善吗？

背景：目前研究多为骨髓间充质干细胞的体外培养及细胞移植对颅内疾病的治疗,对植入细胞在损伤脊髓中的成活、分化、迁移、结构重建等了解有限。 目的：探讨局部骨髓间充质干细胞移植在脊髓损伤修复中的作用和骨髓间充质干细胞替代治疗的可行性。 方法：成年健康雌性SD大鼠随机分为细胞移植组和对照组,建立SD大鼠脊髓横断损伤模型,伤后即刻分别向损伤区局部移植大鼠骨髓间充质干细胞悬液或无钙镁磷酸缓冲液。在术前和术后1 d,1周,2周,3周,4周和8周进行BBB评分,观测大鼠的运动功能,并于移植后1周免疫组织化学染色法观察BrdU标记的骨髓间充质干细胞在脊髓损伤处的存活情况,移植后4周进行损伤脊髓的大体观察和组织学检测。 结果与结论：移植后第1~8周细胞移植组BBB评分均髙于对照组;术后1周免疫组织化学染色结果显示在细胞移植组大鼠脊髓远端检测到BrdU阳性细胞,术后4周脊髓损伤处发现有神经纤维。证实通过损伤后立即局部注射的方式将骨髓间充质干细胞移植进大鼠脊髓损伤区,细胞可在损伤区存活;存活的骨髓间充质干细胞可分化为神经元,在损伤局部形成神经元通路,从而促进脊髓神经纤维传导功能的恢复,并促进高位脊髓损伤后大鼠后肢运动功能恢复。     

骨形态发生蛋白4体内外诱导脑神经干细胞向胆碱能细胞的分化

目的：了解骨形态发生蛋白－4 (BMP4) 是否具有诱导原代分离培养的大鼠脑神经干细胞（NSCs）向胆碱能细胞分化的效应。方法：将从两月龄大鼠脑海马、纹状体等区域分离的细胞培养于含EGF、bFGF的DMEM/F12培养液中,在光镜下观察细胞的形态特征,并行Nestin细胞化学染色。24h后换成含有BMP4的培养液,培养7d、8d时,行胆碱乙酰转移酶（choline acetyltransferase, ChAT）和神经巢蛋白Nestin双标免疫细胞化学染色及ChAT间接免疫荧光染色,在光镜下观察细胞形态的变化。结果：分离出的大鼠脑海马、纹状体等区的细胞约48%为nestin阳性的NSCs。培养7d、8d时,光镜下见加BMP4组约34%的细胞呈神经元形态特征;免疫双标细胞化学染色见ChAT阳性细胞与Nestin阳性细胞共存,其中ChAT阳性细胞占28%,Nestin阳性细胞占38%;间接免疫荧光染色见呈较强绿色荧光的ChAT阳性细胞较多;FITC标记流式细胞术检测到16％的细胞呈ChAT阳性。而未加BMP4组呈ChAT阳性的细胞约7％,明显少于加BMP4组,且荧光较弱。结论：BMP4可在体外培养条件下诱导大鼠脑神经干细胞向胆碱能细胞分化。     

生物素葡聚糖胺皮质脊髓束顺行示踪技术在大鼠脊髓损伤模型中的应用

目的探讨生物素葡聚糖胺(BDA)神经示踪技术及脊髓半横断损伤模型在大鼠脊髓损伤修复的实验研究中应用。方法采用成年Sprague-Dawley大鼠,分为脊髓致伤组(n=10)和致伤对照组(n=10)。致伤组动物在相当于T7椎板水平横行剪断脊髓的后2/3;对照组动物术中仅切除椎板,不切断脊髓。术后第15d,右侧开颅,用10?A示踪剂注入右侧的感觉运动区皮质内。2周后取出大脑和脊髓组织,采用自由漂乳法行BDA染色显影。术后实验动物功能测评采用BBB运动功能评分,所得数据采用Student'st-test进行统计学原理。结果(1)脊髓损伤组动物双后肢瘫痪,BBB运动功能评分明显低于损伤对照组,统计学比较差异十分显著(P<0.01);(2)BDA顺行示踪显示大脑皮层BDA注射区内见大脑皮层的锥体细胞及其发出的轴突呈阳性染色,BDA阳性染色的皮质脊髓束神经纤维在同侧中脑、桥脑及延髓的腹侧面行走,在锥体交叉后皮质脊髓束主要在对侧脊髓白质的后索中行走。在致伤组动物中,位于脊髓白质后索中的皮质脊髓束纤维在脊髓损伤处终止;对照组皮质脊髓束BDA染色可一直延伸至L1水平。结论大鼠半脊髓切断结合应用BDA顺行示踪技术可以对脊髓损伤后的神经修复状况进行可靠的形态学评判,是研究脊髓损伤后中枢神经纤维再生修复较为理想的动物模型     

自体肋间神经联合酸性成纤维细胞生长因子移植治疗高位脊髓损伤

背景：酸性成纤维细胞生长因子具有调节细胞增殖、移行、分化和生存的作用,也可以下调已知轴突再生的抑制因子如蛋白聚糖等,帮助轴突克服这些抑制因子,对神经纤维再生有重要作用。 目的：观察酸性成纤维细胞生长因子联合周围神经移植治疗大鼠高位脊髓损伤的可行性及效果。 方法：健康成年雌性SD大鼠108只随机抽签法分为自体神经组、自体神经联合生长因子组、高位脊髓横断组。咬除大鼠T8~10棘突、椎板,显露硬膜囊,水平切断高位脊髓并切除3 mm,显微镜下确认无神经纤维相连。自体神经组、自体神经联合生长因子组取双侧第8~10对肋间神经各2 cm,将肋间神经交叉移植入高位脊髓缺损处(近端白质与远端灰质、远端白质与近端灰质),分别以纤维蛋白凝胶、含有酸性成纤维细胞生长因子的纤维蛋白凝胶固定植入的肋间神经,缝合硬膜。高位脊髓横断组断端间旷置。术后90 d,行体感诱发电位及运动诱发电位检测观察神经电生理恢复情况。术后76 d,生物素葡聚糖胺顺行神经示踪观察运动传导束恢复情况。术后60 d,后肢BBB运动功能评分观察肢体运动恢复情况。 结果与结论：高位脊髓横断组大鼠均未引出体感及运动诱发电位波形。自体神经组、自体神经联合生长因子组均可引出体感及运动诱发电位,自体神经联合生长因子组体感诱发电位及运动诱发电位的平均潜伏期和波幅、BBB评分均明显优自体神经组(P < 0.01)。自体神经组和自体神经联合生长因子组在损伤区有较多生物素葡聚糖胺标记阳性神经纤维通过,明显多于高位脊髓横断组(P < 0.01),自体神经联合生长因子组多于自体神经组(P < 0.01)。提示自体周围神经移植酸性成纤维细胞生长因子能更好地恢复高位脊髓损伤后大鼠肢体运动功能。     

大鼠脊髓损伤后PLGA支架细胞髓内移植的组织学观察

目的 观察神经干细胞(NSC)、许旺细胞(SCs)和组织工程材料乙交酯-丙交酯共聚物(PLGA)大鼠髓内共移植后的病理形态学改变.方法 36只Wistar大鼠,随机分为PLGA移植组、NSC/PLGA组和NSC+SCs/PLGA组.体外培养、鉴定胚胎脊髓源NSC和SCs,制备和构建PLGA支架细胞复合体并移植到大鼠脊髓Tq半横断损伤部位,应用HE染色、电镜和免疫组织化学染色方法在形态结构上观察材料的组织相容性、轴突髓鞘再生及NSC在脊髓内的存活、迁移和分化情况.结果 HE染色观察损伤12周时移植材料内可见细胞生长及新生的毛细血管;扫描电镜观察随着时间的延长,PLGA逐渐降解;材料正中横断面透射电镜观察可见新牛的无髓及有髓神经纤维;脊髓标本免疫组织化学染色可见移植的NSC可以在宿主脊髓内存活、迁移并分化成类神经元样细胞和少枝胶质细胞,未分化成星形胶质细胞.结论 NSC、SCs和PLGA共移植可以在形态学上促进大鼠脊髓半横断损伤的修复.     

神经干细胞与许旺细胞共移植于大鼠损伤脊髓

目的 观察神经干细胞与许旺细胞共移植于大鼠半横断脊髓损伤处神经干细胞的迁移、存活、分化及对损伤脊髓的修复作用.方法 绿色荧光蛋白(GFP)标记脊髓神经下细胞后与许旺细胞共移植于大鼠半横断脊髓损伤处,免疫荧光染色和电镜技术分别观察神经下细胞的迁移、存活、分化及新生的髓鞘.皮层运动诱发电位(CMEPs)及BBB评分分别检测大鼠运动功能的恢复.结果 在神经干细胞与许旺细胞共移植组,损伤脊髓的头端、尾端及对侧町见明显的GFP阳性细胞及GaLC/GFP、GFAP/GFP、NSE/GFP、SYN/GFP舣阳性细胞,电镜下新生的髓鞘最多,CMEPs恢复百分率和振幅明显高于其他两组,但BBB评分与神经干细胞单移植组差异无统计学意义.结论 神经干细胞和许旺细胞体内共移植可促进神经干细胞的辽移、存活、分化及脊髓运动功能的恢复.     

无细胞神经移植物复合骨髓间充质干细胞构建组织工程人工神经修复坐骨神经缺损

背景：作者前期已经成功将无细胞神经移植物复合骨髓间充质干细胞构建组织工程人工神经,并证明可以促进周围神经再生。 目的：构建组织工程人工神经,观察和验证桥接大鼠坐骨神经缺损后的神经功能恢复情况。 方法：成年雄性SD大鼠60只构建大鼠坐骨神经15 mm缺损模型。随机分成3组,每组20只。桥接大鼠坐骨神经缺损,实验组采用组织工程人工神经,空白对照组采用无细胞组织工程神经支架,自体神经对照组采用自体神经移植。桥接后12周通过大体观察、胫骨前肌湿质量、组织学等方法分析坐骨神经组织学及功能恢复情况。 结果与结论：桥接术后12周：实验组大鼠肢体可以支撑着地,钳夹大鼠手术侧足底皮肤出现逃避反射,足底皮肤s-100蛋白染色呈阳性反应。实验组与自体神经移植组胫骨前肌湿质量比差异无显著性意义(P > 0.05)。实验组辣根过氧化物酶逆行示踪实验显示脊髓、后根神经节均可见数量不等的辣根过氧化物酶标记阳性细胞。实验组移植物与自体神经移植组有髓神经纤维数、髓鞘厚度、神经组织面积比较差异无显著性意义。实验结果验证了无细胞神经移植物复合骨髓间充质干细胞构建组织工程人工神经修复大鼠坐骨神经缺损,可以促进神经组织学的修复重建和功能的恢复。     

The Role of Vasoactive Intestinal Polypeptide and Pituitary Adenylate Cyclase-Activating Polypeptide in the Neural Pathways Controlling the Lower Urinary Tract

Vasoactive intestinal polypeptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP) are expressed in the neural pathways regulating the lower urinary tract. VIP-immunoreactivity (IR) is present in afferent and autonomic efferent neurons innervating the bladder and urethra, whereas PACAP-IR is present primarily in afferent neurons. Exogenously applied VIP relaxes bladder and urethral smooth muscle and excites parasympathetic neurons in bladder ganglia. PACAP relaxes bladder and urethral smooth muscle in some species (pig) but excites the smooth muscle in other species (mouse). Intrathecal administration of VIP in cats with an intact spinal cord suppresses reflex bladder activity, but intrathecal administration of VIP or PACAP in rats enhances bladder activity and suppresses urethral sphincter activity. PACAP has presynaptic facilitatory effects and direct excitatory effects on lumbosacral parasympathetic preganglionic neurons. Chronic spinal cord transection produces an expansion of VIP-IR (cats) and PACAP-IR (rats) in primary afferent axons in the lumbosacral spinal cord and unmasks spinal excitatory effects of VIP on bladder reflexes in cats. Intrathecal administration of PACAP6-38, a PAC1 receptor antagonist, reduces bladder hyperactivity in chronic spinal-cord-injured rats. These observations raise the possibility that VIP or PACAP have a role in the control of normal or abnormal voiding.     

Location and completeness of reinnervation by two types of neurons at a single target: The feline muscle spindle

Muscle spindles from the tenuissimus muscle of the cat were examined microscopically to assess the precision and completeness of reinnervation of intrafusal muscle fibers by efferent and afferent neurons. Positions of motor and sensory nerve terminals were charted relative to the cross-sectional area enclosed by the outer capsule of the spindle. Profiles of nerve endings were measured for normally innervated and reinnervated spindles. The tenuissimus was deprivedof innervation by freezing its nerve, sometimes in conjunction with either spinal ganglion removal or ventral rhizotomy. Sensory and motor terminals occupied separate locales along the length of normal muscle spindles. Nerve terminals of efferent and afferent neurons were located in appropriate positions along the length of spindles when axons of both types of neurons regrew-together and when either category of axon regenerated alone. Precise reinnervation of muscle spindles occurred in spite of a diminished diameter of intrafusal fibers. Repopulation of the spindle with motor endings was less complete than that by sensory endings, based on the proportion and size of the regenerated terminals. We conclude that under optimal conditions for axonal regrowth, efferent and afferent neurons reinnervate their respective regions along intrafusal muscle fibers but motor lags sensory reinnervation within the spindle. The mechanism by which positional specificity happens during reinnervation of intrafusal fibers requires neither an interaction between terminals of the two types of neurons nor target cells of normal bulk. © 1993 Wiley-Liss, Inc.     

Morphological plasticity in efferent pathways to the urinary bladder of the rat following urethral obstruction

Partial urethral ligation in female Wistar rats produces changes in the neural control of the lower urinary tract including bladder hyperactivity and facilitation of a spinal micturition reflex pathway. To gain insight into the mechanisms underlying these changes, axonal tracing studies were conducted to examine the postganglionic efferent limb of the micturition reflex pathway which originates in the major pelvic ganglion (MPG). Forty microliters of the tracer Fluoro-Gold (4%) were injected into the right side of the bladder in urethral-obstructed (n = 10) and control (n = 4) rats 6 weeks after urethral ligation or sham surgery. As a control Fast blue (40 microliters, 5%) was injected into the colon to label neurons in the MPG innervating the intestine. Obstructed rats exhibited a 6-fold increase (p less than 0.001) in bladder weight (0.848 gm) compared to controls (0.148 gm). A significant increase (p less than 0.001) in the size of labeled bladder postganglionic neurons in the MPG was noted in obstructed rats (576.4 microns 2, n = 4) as compared to controls (299.6 microns 2). However, labeled, colon postganglionic neurons in the MPG in obstructed (312.9 microns 2) rats were not enlarged compared to controls (359.4 microns 2). Neuronal hypertrophy was not associated with a change in the number of labeled MPG neurons in control and obstructed groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

BDNF基因修饰神经干细胞移植治疗脊髓损伤的实验研究

目的研究BDNF基因修饰神经干细胞移植对脊髓损伤后神经细胞凋亡的影响。方法采用电控大鼠脊髓损伤打击装置制作大鼠脊髓损伤模型。120只SD大鼠随机分为4组:假手术组(Sham组),脊髓损伤组(SCI组),神经干细胞组(NSC组),BDNF基因修饰神经干细胞组(NSC-BDNF组)。通过免疫组化法检测大鼠脊髓BDNF、Bax、Bcl-2的表达,流式细胞仪检测大鼠脊髓细胞凋亡率。结果NSC-BDNF组中BDNF免疫阳性细胞光密度值较NSC、SCI组增加明显(P<0.05),表达时间及表达高峰延长,且Bcl-2的表达较其他组在各个时间点上均增高(P<0.05),而Bax的表达较其他组在各个时间点上均降低(P<0.05),凋亡率亦明显低于NSC和SCI组(P<0.01)。结论BDNF基因修饰神经干细胞移植可引起BDNF在损伤脊髓内有效表达,且明显的促进了脊髓损伤后Bcl-2的高表达,抑制了Bax的表达,从而降低了神经细胞的凋亡率。     

The contribution of capsaicin-sensitive innervation to activation of the spinal vesico-vesical reflex in rats: relationship between substance P levels in the urinary bladder and the sensory-efferent function of capsaicin-sensitive sensory neurons

In acute spinal rats (C2-C3) the transvesical infusion of saline activates a vesico-vesical excitatory reflex (Brain Res., 380 (1986) 83-93). In bladders containing a subthreshold amount of fluid the topical application of capsaicin on the outer surface of the bladder dome activated this spinal reflex and also produced a transient rise in blood pressure and heart rate. The effects of systemic capsaicin desensitization (50 mg/kg s.c. 5 min, 60 days before) on the sensory (activation of the spinal vesico-vesical reflex) and 'efferent' (tetrodotoxin-insensitive capsaicin-induced contraction) functions mediated by the capsaicin-sensitive sensory fibers were correlated to changes in substance P-like immunoreactivity (SP-LI) content of the urinary bladder in adult rats. Blockade of both sensory and efferent functions was observed at a time (60 min from capsaicin administration) when the SP-LI content of the urinary bladder was unaffected. Four days after capsaicin desensitization the SP-LI levels of the bladder are almost depleted indicating that the neuropeptide(s) are entirely stored in sensory structures. At this time the sensory-efferent functions mediated by these fibers are still blocked. At 15-60 days from systemic capsaicin desensitization there was a progressive, time-related recovery of SP-LI levels in the bladder as well as of the sensory-efferent functions. These findings indicate a role of the capsaicin-sensitive innervation of the urinary bladder in activating the spinal vesico-vesical reflex. The present findings suggest that measurement of SP-LI levels in the rat bladder may be a useful biochemical index for monitoring the function(s) of the capsaicin-sensitive, peptidergic sensory neurons.     

Anatomical evidence for two spinal 'afferent-interneuron-efferent' reflex pathways involved in micturition in the rat: a 'pelvic nerve' reflex pathway and a 'sacrolumbar intersegmental' reflex pathway

We labeled interneurons in the L1-L2 and L6-S1 spinal cord segments of the rat that are involved in bladder innervation using transneuronal retrograde transport of pseudorabies virus (PRV) in normal animals and in animals with selected nerve transections. Preganglionic neurons were identified using antisera against choline acetyltransferase (ChAT). In some experiments we labelled parasympathetic preganglionic neurons (PPNs) in the L6-S1 spinal cord by retrograde transport of Fluorogold from the major pelvic ganglion. We identified bladder afferent terminals using the transganglionic transport of the anterograde tracer cholera toxin subunit b. We present anatomical evidence for two spinal pathways involved in innervation of the bladder. First, in the intact rat, afferent information from the bladder connects, via interneurons in L6-S1, to the PPNs that provide the efferent innervation of the bladder. The afferent terminals were located mainly in close apposition to interneurons located dorsal to the retrogradely labeled PPNs. Second, using L6-S1 ganglionectomies or L6-S1 ventral root rhizotomies we limited viral transport to the sympathetic pathways innervating the bladder. This procedure also labelled interneurons (but not PPNs) with PRV in the L6-S1 spinal cord in a location very similar to those described in the intact rat. These interneurons also receive bladder afferent terminals but we propose that they project to sympathetic preganglionic neurons, most of which are in the L1-L2 spinal segments. Based on this anatomical evidence, we propose the existence of two spinal reflex pathways involved in micturition: a pathway limited to a reflex arc in the pelvic nerve (presumably excitatory to the detrusor muscle); and a pathway involving the pelvic nerve and sympathetic nerve fibers, some of which may travel in the hypogastric (presumably inhibitory to the detrusor muscle).     

Degeneration of vagal efferent axons and terminals in cardiac ganglia of aged rats

Baroreflex control of the heart rate is significantly reduced during aging. However, neural mechanisms that underlie such a functional reduction are not fully understood. We injected the tracer DiI into the left nucleus ambiguus (NA), then used confocal microscopy and a Neurolucida Digitization System to examine qualitatively and quantitatively vagal efferent projections to cardiac ganglia of young adult (5-6 months) and aged (24-25 months) rats (Sprague Dawley). Fluoro-Gold was injected intraperitoneally to counterstain cardiac ganglionic principal neurons (PNs). In aged, as in young rats, NA axons projected to all cardiac ganglia and formed numerous basket endings around PNs in the hearts. However, significant structural changes were found in aged rats compared with young rats. Vagal efferent axons contained abnormally swollen axonal segments and exhibited reduced or even absent synaptic-like terminals around PNs, such that the numbers of vagal fibers and basket endings around PNs were substantially reduced (P < 0.01). Furthermore, synaptic-like varicose contacts of vagal cardiac axons with PNs were significantly reduced by approximately 50% (P < 0.01). These findings suggest that vagal efferents continue to maintain homeostatic control over the heart during aging. However, the marked morphological reorganization of vagal efferent axons and terminals in cardiac ganglia may represent the structural substrate for reduced vagal control of the heart rate and attenuated baroreflex function during aging.     

Neural pathways of somatic and visceral reflexes of the external urethral sphincter in female rats

The external urethral sphincter (EUS) plays a crucial role in maintaining urinary continence. The activity of the EUS is modulated by bladder and urethra sensory neurons. However, a complete understanding of the somatic or visceral sources that modulate the EUS is lacking. The aims of the present study were to characterize the response of the EUS to perineal skin, genital, rectal, and urethral mechanical stimulation, as well as to determine the peripheral neural pathways of the reflex. EUS reflex electromyographic activity (EMG), innervation of pelvic and perineal structures, and the anatomy of afferent and efferent nerves were determined in anesthetized female rats. The EUS responds to cutaneous as well as genital and rectal stimuli. However, the EUS EMG response is significantly larger when induced by genital stimulation. The dorsal nerve of the clitoris and the cavernous nerve both innervate the distal urethra and the distal vagina, as well as the clitoris and perigenital skin and are the main afferent pathways for the genito‐sphincteric reflex. Efferent axons travel through the pudendal nerve and the lumbosacral trunk and converge in the motor branch of the lumbosacral plexus, which innervates the EUS. Because the nerves are located on the vaginal walls, they are susceptible to damage during childbirth. Physiology and anatomy of the different neural pathways that regulate EUS activity are important to consider when inducing nerve damage to create models of urinary incontinence. J. Comp. Neurol., 520:3120–3134, 2012. © 2012 Wiley Periodicals, Inc.     

Role of somatic afferents in autonomic system control of the intestinal motility

(1) In anesthetized (chloralose-urethane) rats, strong mechanical stimuli which were applied to the abdominal skin always inhibited motility of the small intestine. This reflex is referred to as an 'inhibitory cutaneo-intestinal reflex'. Similar stimuli applied to the skin of the upper chest, neck, forepaws, or hindpaws, however, evoked the opposite effect, which is referred to as a 'facilitatory cutaneo-intestinal reflex'. (2) By recording the activity of efferent sympathetic nerves to the small intestine and by transecting intestinal sympathetic or parasympathetic nerves we found that the inhibitory cutaneo-intestinal reflex was largely due to an increase in intestinal sympathetic efferent activity, and that the facilitatory cutaneo-intestinal reflex was due to decrease in the intestinal sympathetic efferent nerve activity; both changes reflexly evoked. (3) The inhibitory cutaneo-intestinal reflex was shown to be a propriospinal reflex which was caused by excitation of group IV (unmyelinated) cutaneous afferent nerve fibers. On the other hand, the facilitatory cutaneo-intestinal reflex seemed to be mediated through supraspinal pathways, and was evoked by excitation of mainly group III (A-delta group) cutaneous afferent nerve fibers. (4) Interaction between the cutaneo-intestinal reflex and intestino-intestinal reflex was demonstrated. (5) The possibility of a dorsal root reflex contribution to cutaneo-intestinal reflex was eliminated. (6) Significance of the cutaneo-intestinal reflex in neural control of the gastro-intestinal tract was discussed.