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This Article Full Text Full Text (PDF) All Versions of this Article: 292/6/F1791    most recent 00443.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by Liao, J.-M. Articles by Lin, T.-B. Search for Related Content PubMed PubMed Citation Articles by Liao, J.-M. Articles by Lin, T.-B.

Spinal glutamatergic NMDA-dependent pelvic nerve-to-external urethra sphincter reflex potentiation caused by a mechanical stimulation in anesthetized rats

¹Department of Physiology, College of Medicine and ⁷Department of Obstretics and Gynecology, Chung-Shan Medical University Hospital, Chung-Shan Medical University, Taichung; ²Department of Life Science, National Chung-Hsing University, Taichung; ³School of Medicine, Kao-Hsiung Medical University, Kaohsiung; Departments of ⁴Biotechnology and ⁵Biomedical Engineering, Ming-Chuan University, Taoyuan; ⁶Department of Veterinary Medicine, College of Veterinary Medicine, Chung-Hsing University, Taichung, Taiwan; and ⁸Department of Medical Education, Saint Paul's Hospital, Taoyuan, Taiwan

Submitted 7 November 2006 ; accepted in final form 5 January 2007

The current study investigates whether the spinal pelvic nerve-to-external urethra sphincter (EUS) reflex potentiation can be induced by a mechanical stimulation and whether the glutamatergic mechanism is involved in yielding such a reflex potentiation. 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 (620 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 µM, 10 µl, 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 µM, 10 µl, 26.16 ± 7.27 spikes/stimulation], but was not affected by bicuculline (a GABAergic antagonist; 100 µM, 10 µl, 53.62 ± 15.54 spikes/stimulation). Intrathecal administration of glutamate (31.12 ± 8.25 spikes/stimulation, 100 µM, 10 µl) and NMDA (26.25 ± 4.12 spikes/stimulation, 100 µM, 10 µl) 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.

pelvic nerve; urethra; LTP; AMPA

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