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Without saline distension (0 cmH<jats:sub>2<\/jats:sub>O), a single pulse nerve stimulation evoked a single action potential in the reflex activity, whereas repetitive pelvic stimulation and saline distension (6\u223c20 cmH<jats:sub>2<\/jats:sub>O) both elicited a long-lasting reflex potentiation (20.05 \u00b1 3.21 and 75.01 \u00b1 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 \u03bcM, 10 \u03bcl, 1.72 \u00b1 0.31 spikes\/stimulation] and attenuated by 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo (F) quinoxaline [NBQX; a glutamatergic \u03b1-amino-3-hydroxy-5-methyl-4-isoxazoleproprionate (AMPA) receptor antagonist; 100 \u03bcM, 10 \u03bcl, 26.16 \u00b1 7.27 spikes\/stimulation], but was not affected by bicuculline (a GABAergic antagonist; 100 \u03bcM, 10 \u03bcl, 53.62 \u00b1 15.54 spikes\/stimulation). Intrathecal administration of glutamate (31.12 \u00b1 8.25 spikes\/stimulation, 100 \u03bcM, 10 \u03bcl) and NMDA (26.25 \u00b1 4.12 spikes\/stimulation, 100 \u03bcM, 10 \u03bcl) 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.<\/jats:p>","DOI":"10.1152\/ajprenal.00443.2006","type":"journal-article","created":{"date-parts":[[2007,2,8]],"date-time":"2007-02-08T01:07:54Z","timestamp":1170896874000},"page":"F1791-F1801","source":"Crossref","is-referenced-by-count":19,"title":["Spinal glutamatergic NMDA-dependent pelvic nerve-to-external urethra sphincter reflex potentiation caused by a mechanical stimulation in anesthetized 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