Effects of NK1 receptor on Repetitive Stimulation-Induced Pelvic-Urethra Reflex Potentiation in Anesthetized Rats

• Main Authors: Hui-Fang Chiu, 邱惠芳
• Other Authors: Cheng-Hui Lin
• Format: Others
• Language: zh-TW
• Published: 2008
• Online Access: http://ndltd.ncl.edu.tw/handle/44599978441776418999

碩士 === 國立臺灣海洋大學 === 水產養殖學系 === 96 === Neurokinin 1 (NK1) receptors are expressed in dorsal horn neurons is recognized to mediate the transmission and modulation of nociception at the spinal cord level. However, the possibility that the NK1 receptor and the downstream intracellular cascade may modulate the induction of the spinal reflex potentiation (SRP), a novel form of activity-dependent neural plasticity mediating post-inflammatory hypergesia and tactile allodynia, has been yet to be established. We test the hypothesis that NK1 and the downstream intracellular PLC/Ca2+ cascade may modulate the induction of SRP using pharmacological approach in in vivo animal preparations. When compared with test stimulation (1/30 Hz) evoked a baseline reflex activity with a single action potential, repetitive stimulation (1 Hz) induced SRP in the reflex activity. Intrathecal Substance P, a Neurokinin 1 receptor agonists (0.1μM, 10μl), induced excitatory effects on the test stimulation (TS, 1/30 Hz) elicited reflex activities, exhibited inhibitory effects reversed by intrathecal Neomycin, a phospholipase C inhibitor (100μM, 10μl). The reversal effect on SRP caused by the Neomycin was reactivation by intrathecal Caffeine, an intracellular calcium release (100μM, 10μl). Intrathecal Hemokinin 1, a Neurokinin 1 receptor agonists (0.1μM, 10μl), induced excitatory effects on the test stimulation (TS, 1/30 Hz) elicited reflex activities, exhibited inhibitory effects reversed by intrathecal Neomycin, a phospholipase C inhibitor (100μM, 10μl). The reversal effect on SRP caused by the Neomycin was reactivation by intrathecal Caffeine, an intracellular calcium release (100μM, 10μl). Intrathecal WIN51708, a NK1 receptor antagonist (100μM, 10μl), exhibited inhibitory effects on the RS-induced SRP that was reversed by intrathecal m-3M3FBS, a phospholipase C activator (100μM, 10μl). The reversal effect on SRP caused by the m-3M3FBS was abolished by intrathecal Dantrolene, an intracellular calcium blocker (100μM, 10μl). These findings suggested that through the Ca2+ release triggered by the phospholipase C activation activating, NK1 receptor may modulate the repetitive stimulation-induced SRP, which is presumed to be involved in post-inflammatory hypergesia and tactile allodynia.