Kijima Hiroshi, Shingai Tomio, Takahashi Yoshihiro, Kajii Yuka, Fukushima Shin-ichi, Taguchi Yo, Noda Tadashi, Yamada Yoshiaki
Division of Pediatric Dentistry, Niigata University Graduate School of Medical and Dental Sciences, 2-5274 Gakkocho-dori, Niigata 951-8514, Japan.
Am J Physiol Regul Integr Comp Physiol. 2006 Sep;291(3):R651-6. doi: 10.1152/ajpregu.00646.2005. Epub 2006 Apr 6.
The pharynx is very important for elicitation of reflex swallowing. The region of the pharynx is innervated by the pharyngeal branch of the glossopharyngeal nerve (GPN-ph). Nitric oxide (NO) plays an important role in various physiological functions. The purpose of this study is to investigate the contribution of NO to reflex swallowing evoked by electrical stimulation of the GPN-ph. Swallowing was evoked in urethane-anesthetized rats by application of repetitive electrical stimulation (10- to 20-microA amplitude, 10- to 20-Hz frequency, 1.0-ms duration) to the central cut end of the GPN-ph or superior laryngeal nerve. Swallowing was identified by electromyographic activity of the mylohyoid muscle. Latency to the first swallow and the interval between swallows were measured. Intravenous administration of N(G)-nitro-L-arginine (L-NNA, 0.6 mg/kg), a nonselective inhibitor of NO synthase (NOS), extremely prolonged latency to the first swallow and the interval between swallows evoked by the GPN-ph. Intraperitoneal administration of 7-nitroindazole (5.0 mg/kg), a selective inhibitor of neuronal NOS, significantly prolonged latency to the first swallow and the interval between swallows evoked by the GPN-ph. Administration of L-arginine (an NO donor, 500 mg/kg) and sodium nitroprusside (an NO releaser, 0.6 mg/kg) restored the suppression of swallowing induced by the NOS inhibitor. Superior laryngeal nerve-evoked swallowing was suppressed by administration of a higher dose of L-NNA (6.0 mg/kg). Swallowing evoked by water stimulation of the pharynx was also suppressed by L-NNA (0.6 mg/kg). These results suggest that NO plays an important role in signal processing for initiation of reflex swallowing from the pharynx.
咽对于引发反射性吞咽非常重要。咽区域由舌咽神经的咽支(GPN-ph)支配。一氧化氮(NO)在各种生理功能中起重要作用。本研究的目的是探讨NO对舌咽神经咽支电刺激诱发的反射性吞咽的作用。通过对舌咽神经咽支或喉上神经的中枢切断端施加重复性电刺激(幅度10至20微安,频率10至20赫兹,持续时间1.0毫秒),在氨基甲酸乙酯麻醉的大鼠中诱发吞咽。通过下颌舌骨肌的肌电图活动来识别吞咽。测量首次吞咽的潜伏期和吞咽之间的间隔。静脉注射一氧化氮合酶(NOS)的非选择性抑制剂N(G)-硝基-L-精氨酸(L-NNA,0.6毫克/千克),极大地延长了舌咽神经咽支诱发的首次吞咽潜伏期和吞咽之间的间隔。腹腔注射神经元型NOS的选择性抑制剂7-硝基吲唑(5.0毫克/千克),显著延长了舌咽神经咽支诱发的首次吞咽潜伏期和吞咽之间的间隔。给予L-精氨酸(一种NO供体,500毫克/千克)和硝普钠(一种NO释放剂,0.6毫克/千克)可恢复NOS抑制剂对吞咽的抑制作用。给予更高剂量的L-NNA(6.0毫克/千克)可抑制喉上神经诱发的吞咽。L-NNA(0.6毫克/千克)也可抑制咽部水刺激诱发的吞咽。这些结果表明,NO在咽部反射性吞咽起始的信号处理中起重要作用。