Spinal glutamatergic NMDA-dependent pelvic nerve-to-external urethra sphincter reflex potentiation caused by a mechanical stimulation in anesthetized rats
Spinal glutamatergic NMDA-dependent pelvic nerve-to-external urethra sphincter reflex potentiation caused by a mechanical stimulation in anesthetized rats
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DOI：
10.1152/ajprenal.00443.2006
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发表时间：
2007-06-01
影响因子：
4.2
通讯作者：
Lin, Tzer-Bin
中科院分区：
文献类型：
--
作者：
Liao, Jiuan-Miaw;Huang, Pei-Chen;Lin, Tzer-Bin
目前的研究调查是否脊髓盆神经外尿道括约肌（EUS）反射增强可以通过机械刺激引起的，以及是否在产生这样的反射增强的mammatergic机制。在30只麻醉大鼠中，记录了单次或重复刺激盆神经诱发的外尿道括约肌肌电图（EUSE）活动。在没有生理盐水扩张（0 cmH（2）O）的情况下，单脉冲神经刺激在反射活动中诱发单个动作电位，而重复骨盆刺激和生理盐水扩张（6类似于20 cmH（2）O）均诱发持久的反射增强（分别为20.05 +/- 3.21和75.01 +/- 9.87尖峰/刺激）。盐水扩张诱导的盆腔神经至EUS反射增强被D-2-氨基-5-磷酸戊酸酯[APV;一种谷氨酸能N-甲基-D-天冬氨酸（NMDA）受体拮抗剂; 100 μ M，10 μ l，1.72 +/- 0.31尖峰/刺激]消除，并被2，3-二羟基-6-硝基-7-氨磺酰基苯并（F）喹喔啉[ NBQX; α-氨基-3-羟基-5-甲基-4-异恶唑丙酸盐（AMPA）受体拮抗剂; 100 μ M，10 μ l，26.16 +/- 7.27峰/刺激]，但不受荷包牡丹碱影响（GABA能拮抗剂; 100 μ M，10 μ l，53.62 +/- 15.54峰/刺激）。鞘内注射谷氨酸（31.12 +/- 8.25峰/刺激，100 μ M，10 μ l）和NMDA（26.25 +/- 4.12峰/刺激，100 μ M，10 μ l）均诱导了持久的盆腔神经-EUS反射增强，而无盐水扩张，这与仅用盐水扩张观察到的结果相似。生理盐水扩张引起的骨盆神经-EUS反射增强延长了尿道收缩波的持续时间，而收缩波的峰值压力不受影响。我们的研究结果表明，在膀胱的盐水扩张elevants盆神经EUS反射增强和mammatergic机制有助于这种反射增强的存在。
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 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.