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dc.contributor.authorLiao, J.M.en_US
dc.contributor.authorHuang, P.C.en_US
dc.contributor.authorPan, S.F.en_US
dc.contributor.authorChen, M.J.en_US
dc.contributor.authorTung, K.C.en_US
dc.contributor.authorPeng, H.Y.en_US
dc.contributor.authorShyu, J.C.en_US
dc.contributor.authorLiou, Y.M.en_US
dc.contributor.authorChen, G.D.en_US
dc.contributor.authorLin, T.B.en_US
dc.description.abstractThe 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 cmH(2)O), a single pulse nerve stimulation evoked a single action potential in the reflex activity, whereas repetitive pelvic stimulation and saline distension (6 similar to 20 cmH(2)O) 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 mu M, 10 mu l, 1.72 +/- 0.31 spikes/stimulation] and attenuated by 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo ( F) quinoxaline [ NBQX; a glutamatergic alpha-amino-3-hydroxy-5-methyl-4- isoxazoleproprionate ( AMPA) receptor antagonist; 100 mu M, 10 mu l, 26.16 +/- 7.27 spikes/stimulation], but was not affected by bicuculline (a GABAergic antagonist; 100 mu M, 10 mu l, 53.62 +/- 15.54 spikes/stimulation). Intrathecal administration of glutamate (31.12 +/- 8.25 spikes/stimulation, 100 mu M, 10 mu l) and NMDA (26.25 +/- 4.12 spikes/stimulation, 100 mu M, 10 mu l) 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.en_US
dc.relationAmerican Journal of Physiology-Renal Physiologyen_US
dc.relation.ispartofseriesAmerican Journal of Physiology-Renal Physiology, Volume 292, Issue 6, Page(s) F1791-F1801.en_US
dc.subjectlong-term potentiationen_US
dc.subjectlower urinary-tracten_US
dc.subjectmicturition reflexen_US
dc.subjectreceptor antagonistsen_US
dc.subjectalpha-amino-3-hydroxy-5-methylisoxazole-4-propionic aciden_US
dc.subjectbladder contractionen_US
dc.subjectdorsal hornen_US
dc.titleSpinal glutamatergic NMDA-dependent pelvic nerve-to-external urethra sphincter reflex potentiation caused by a mechanical stimulation in anesthetized ratsen_US
dc.typeJournal Articlezh_TW
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