Holmes G M, Hermann G E, Rogers R C, Bresnahan J C, Beattie M S
Department of Neuroscience, Ohio State University, 4068 Graves Hall, 333 West Tenth Avenue, Columbus, OH 43210-1239, USA.
Physiol Behav. 2002;75(1-2):49-55. doi: 10.1016/s0031-9384(01)00631-x.
Rat preparations were used to investigate long-term changes in external anal sphincter (EAS) contractions and reflexive penile erection following electrolytic lesions of the nucleus raphe obscurus (nRO) or the rostral ventrolateral medulla. EAS contractions were measured electromyographically (EAS EMG) following distention of the EAS with a 5-mm probe. Penile erections were measured using a standard ex copula reflex testing paradigm. At 48 h postlesion, 100% of nRO-lesioned animals displayed reflexive erections and the magnitude of EAS EMG was significantly greater in lesioned animals than in sham controls. These results suggested EAS hyperreflexia following destruction of the nRO. By 14 days postlesion, EAS responsiveness in nRO-lesioned animals had returned to levels comparable to nonlesioned animals. No measures of penile erection were affected by nRO lesions. In animals with nucleus gigantocellularis (Gi) and lateral nucleus paragigantocellularis (Gi-lPGi) lesions, no significant changes to EAS reflexes were observed at any time point. At 48 h postoperative, Gi-lPGi lesions significantly reduced the latency to first erection and increased the number of erections elicited relative to controls. Similar facilitation of erection latency was observed at 14 days postlesion, while erection number and flip total were no longer significantly different from controls. These and previous studies suggest that the nRO regulates defecatory reflexes in the rat. These data further suggest that the comingled EAS and bulbospongiosus (BS) motoneurons are controlled by discrete and separate brainstem circuits and that increases in EAS and penile reflexes after spinal cord lesions are mediated by loss of different descending inputs.
采用大鼠制备模型,研究中缝隐核(nRO)或延髓头端腹外侧区电解损伤后肛门外括约肌(EAS)收缩和反射性阴茎勃起的长期变化。用5毫米探头扩张EAS后,通过肌电图(EAS EMG)测量EAS收缩。使用标准的交配后反射测试范式测量阴茎勃起。损伤后48小时,100%的nRO损伤动物表现出反射性勃起,且损伤动物的EAS EMG幅度显著大于假手术对照组。这些结果提示nRO破坏后EAS反射亢进。损伤后14天,nRO损伤动物的EAS反应性已恢复到与未损伤动物相当的水平。nRO损伤未影响阴茎勃起的各项指标。在巨细胞网状核(Gi)和外侧旁巨细胞网状核(Gi-lPGi)损伤的动物中,在任何时间点均未观察到EAS反射有显著变化。术后48小时,Gi-lPGi损伤显著缩短首次勃起的潜伏期,并增加相对于对照组诱发的勃起次数。在损伤后14天观察到类似的勃起潜伏期缩短,而勃起次数和翻转总数与对照组不再有显著差异。这些研究及之前的研究表明,nRO调节大鼠的排便反射。这些数据进一步表明,混合的EAS和球海绵体肌(BS)运动神经元由离散且独立的脑干回路控制,脊髓损伤后EAS和阴茎反射的增强是由不同下行输入的丧失介导的。