| Summary: | 碩士 === 中山醫學大學 === 醫學研究所 === 94 === The aim of this study was to examine the participation of nitrinergic neurotransmission in the stimulation-induced potentiation on pelvic nerve-to-urethra reflex (PUR) activities and determine the neuronal nitric oxide synthase (nNOS) reactivity of lower spinal levels (L6-S2), which mediated micturition function after total sleep deprivation (TSD).The magnitude of the repetitive stimulation (RS, 1 Hz)-induced potentiation in PUR activity decreased significantly in the TSD group when compared with the control groups (19.86±1.39 and 9.43±1.39 spikes/stimulation in control and TSD group; respectively, P < 0.01, n=7). The magnitude of the RS induced potentiation in PUR activity decreased significantly after intrathecal 6-Cyano-7-nitroquinoxaline-2,3-dione (CNQX; from 15.36±1.11 to 7.21±0.74, and from 9.44±0.44 to 5.44±0.58 spikes/stimulation in control, and TSD, respectively, P<0.01, n=7) and D-2-amino-5-phosphonoraleric acid (APV, from 17.38±1.30 to 2.94±0.34, and from 9.44±0.44 to 2.25±0.31 spikes/stimulation in control, and TSD, respectively, P < 0.01, n=7). In addition, potentiation in PUR activities was induced by intrathecal L-glutamate (from 1.50±0.22 to 26.50±0.50, and from 1.33±0.21 to 5.67±0.42 spikes/stimulation in control, and TSD, respectively, P < 0.01, n=7) and N-methyl-Daspartic acid (from 1.17±0.17 to 11.50±1.50, and from 1.33±0.21 to 3.83±0.40 spikes/stimulation in control, and TSD); Intrathecal L-NAME blocked repetitive stimulation induced potentiation in pelvic-urethral reflex activities (from 14.56±0.80 to 3.67±0.71, and from 9.33±0.33 to 3.67±0.33 spikes/stimulation in control, and TSD P<0.01, n=7). Intrathecal L-Arg reversed the blocking effects exerted by L-NAME on repetitive stimulation-induced pelvic-urethral reflex potentiation (from 3.67±0.71 to 14.17±1.19, and from 3.67±0.33 to 9.67±0.33 spikes/stimulation in control, and TSD P<0.01, n=7).
nNOS activities were found in the lower spinal levels. In addition, following TSD treatment, the intensity of nNOS reactivity were reduced when compared with control group (n=5). All the results suggest that the increased nNOS in spinal levels appears to be related with the RS-induced potentiation in PUR activity and decrease of nNOS expression may deteriorate the spinal neurotransmission and result in the TSD-induced micturition dysfunction.
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