Nitric oxide inhibits excitatory vagal afferent input to nucleus tractus solitarius neurons in anaesthetized rats

一氧化氮抑制迷走神经介导的孤束核神经元兴奋性传入(英文)

Objective Endogenous nitric oxide （NO） has been implicated in the regulation of neuronal activity which mediates cardiovascular reflexes. However, there is controversy concerning the role of NO in the nucleus tractus solitarius （NTS）. The present study aims to elucidate the possible physiological role of endogenous NO in modulating the excitatory vagal afferent input to NTS neurons. Methods All the experiments in the rat were conducted under anaesthetic conditions. Ionophoresis method was used for the application of NO donor or nitric oxide synthase （NOS） inhibitor, and single unit recording method was employed to detect the effects of these applications on vagal afferentor cardio-pulmonary C-fibre reflex-evoked neuronal excitation in NTS. Results Ionophoresis applications of L-arginine （L-Arg）, a substrate of NOS, and sodium nitroprusside （SNP）, a NO donor, both attenuated the vagal afferent-evoked discharge by （51.5±7.6）% （n = 17） and （68.3±7.1）% （n = 9）, respectively. In contrast, application of D-Arg at the same current exerted no overall effect on this input. Also, both L-Arg and SNP inhibited spontaneous firing of most of the recorded neurons. In contrast, ionophoresis application of NG-nitro-Larginine methyl ester （L-NAME） enhanced vagal afferent-evoked excitation by （66.3±11.4）% （n = 7）. In addition, ionophoresis application of L-Arg and SNP significantly attenuated cardio-pulmonary C-fibre reflex-induced excitation in the tested NTS neurons. Conclusion Activation of local NO pathway in the NTS could suppress vagal afferent-evoked excitation, suggesting that NO is an important neuromodulator of visceral sensory input in the NTS.

目的一氧化氮在延髓孤束核内调控心血管反射功能的确切机制尚未得到阐明。本实验将微电泳与细胞外神经元记录技术结合,研究一氧化氮对孤束核神经元接受迷走神经介导的兴奋性传入的调控作用,揭示一氧化氮在延髓孤束核内调控心血管反射的重要作用。方法将大鼠进行整体麻醉,通过单细胞记录孤束核神经元的电活动。微电泳给予一氧化氮供体或一氧化氮合成酶抑制剂,观察其对迷走神经电刺激或肺化学感受器刺激下诱发的孤束核神经元兴奋性反应的调控作用。结果微电泳给予L-arginine(L-Arg)或硝普纳均能抑制迷走神经刺激诱发的孤束核神经元兴奋反应,分别降低了(51.5±7.6)%(n=17)和(68.3±7.1)%(n=9)。而在相同条件下给予D-Arg并未出现任何影响。并且在大部分所测神经元中,L-Arg和硝普纳均能抑制神经元的自放电行为。相反,微电泳给予L-NAME则会加强迷走神经刺激诱发的孤束核神经元兴奋反应,增强了(66.3±11.4)%(n=7)。另外,微电泳给予L-Arg或硝普纳都能抑制肺化学感受器刺激下诱发的孤束核神经元兴奋性反应。结论在延髓孤束核内一氧化氮对迷走神经介导的心血管反射具有负调控作用。