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1 Department of Physiology, College of Medicine, Chung-Shan Medical University, Chung-Shan Medical University, No. 110 Chang-Kuo North Rd. the first Section Taichung, Taiwan 10018, Taichung, 40201
2 School of Medicine, Kao-Hsiung Medical University, United States
3 Ming-Chuan University, Department of Biotechnology, United States
4 Ming-Chuan University, Department of Biomedical Engineering, United States
5 Institue of Veterinary Medicine, College of Veterinary Medicine, Chung-Hsing University, United States
6 Department of Physiology, College of Medicine, Chung-Shan Medical University, Taichung, United States
7 Chung-Shan Medical University Hospital, Department of Physiology, College of Medicine, United States
8 National Chung-Hsing University, bDepartment of Life Science, United States
9 Chung-Shan Medical University Hospital, Department of Obstretics and Gynecology, United States
10 Department of Physiology, College of Medicine, Chung-Shan Medical University, Tai-Chung, United States
* To whom correspondence should be addressed. E-mail: tblin{at}csmu.edu.tw.
The current study investigates whether the spinal pelvic nerve-to-external urethra sphincter (EUS) reflex potentiation can be induced by a mechanical stimulation. The external urethra sphincter electromyogram (EUSE) activity, evoked by a single or by repetitive pelvic nerve stimulation, in 30 anesthetized rats was recorded with/without bladder saline distension. Without saline distension (0 cmH2O), a single pulse nerve stimulation evoked a single action potential in the reflex activity, whereas repetitive pelvic stimulation and saline distension (6~20 cmH2O) both elicited a long-lasting reflex potentiation (20.05±3.21 and 75.01±9.87 spikes/stimulation, respectively). The saline distension-induced pelvic nerve-to-EUS reflex potentiation was abolished by D-2-amino-5-phosphonovalerate [APV, a glutamatergic N-methyl-D-aspartic acid (NMDA) receptor antagonist; 100 uM, 10 ul, i.t., 1.72±0.31 spikes/stimulation] and attenuated by 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo (F) quinoxaline [NBQX, a glutamatergic 
-amino-3-hydroxy-5-methyl-4-isoxazoleproprionate (AMPA) receptor antagonist; 100 uM, 10 ul, i.t., 26.16±7.27 spikes/stimulation], but was not affected by bicuculline (a GABAergic antagonist; 100 uM, 10 ul, i.t., 53.62±15.54 spikes/stimulation). Intrathecal administration of glutamate (31.12±8.25 spikes/stimulation, 100 uM, 10 ul) and NMDA (26.25±4.12 spikes/stimulation, 100 uM, 10 ul) both induced a long-lasting pelvic nerve-to-EUS reflex potentiation without saline distension, which was similar to the findings observed from saline distension only. The duration of the contraction wave of the urethra was elongated by the saline distension-induced pelvic nerve-to-EUS reflex potentiation, whereas the peak pressure of the contraction wave was not affected. Our findings suggest that saline distension in the bladder elicits a pelvic nerve-to-EUS reflex potentiation and the glutamatergic mechanism contributes to the presence of such a reflex potentiation.
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