NITRIC OXIDE ON ACUPUNCTURE SIGNALS IN GRACILE NUCLEUS

后肢低频电针刺激(EA) 穴位在人类和大鼠身上产生长期的交感抑制。这个 薄束核接受从后肢投射的初级传入纤维。 刺激躯体感觉神经引起交感神经变化 活动和动脉血压。我们发现神经性一氧化氮 老年细小核合酶表达明显增加 Fischer大鼠和自发性高血压大鼠降低。我们最近的研究 结果表明，低频刺激可增强小脑束核中nNOS的表达 针刺大鼠后肢穴位并伴有nNOS升高 蛋白质水平。初步结果表明，微量注射A或A 一氧化氮(NO)供体或L-精氨酸进入薄束核改变 电针刺激穴位的心血管反应。脊椎前突 位于薄束核中的束细胞由单一的电信号激活 通过背侧传递突触时对坐骨神经的刺激 柱被伽马氨基丁酸(GABA)介导的去极化抑制 温文尔雅的来访者。 拟议研究的目的是研究我们的假设，即EA 刺激后肢穴位诱导大鼠脑内nNOS表达上调 纤细核和nNOS-NO-GABA系统起抑制作用 小脑-丘脑通路中心血管功能的调节。这个 主要目的是确定：1)松弛核中的NO是否改变了 电针对后肢穴位的交感神经和心血管反应？ 2)GABA能传递是否介导了NO对电针的抑制反应 在薄束核中的刺激？3)对 电针诱导的内源性NO释放在薄束核平行于交感神经。 和心血管反应？4)nNOS在薄束核中表达 EA有选择地上调监管？和5)什么是分布的 电针诱导丘脑薄层通路中Fos/nNOS的表达这个 动脉血压、心率和肾脏的生理记录 交感神经活动将与电针刺激和 神经药理学操作和组织化学研究以测试 大鼠模型中的假说。 这些结果应该会促进我们对这些地点和影响的理解 低频电针后肢穴对大鼠神经元型一氧化氮合酶的调节 并对NO和NO的中枢机制产生了新的见解 电针对交感神经的抑制作用。

Low-frequency electroacupuncture (EA) stimulation of hindlimb acupoints produces long-lasting sympathoinhibition in humans and rats. The gracile nucleus receives primary afferents projecting from the hindlimb, and stimulation of somatic sensory nerves results in changes in sympathetic nerve activity and arterial blood pressure. We have found that neuronal nitric oxide synthase (nNOS) expression in the gracile nucleus is markedly increased in old Fischer rats and reduced in spontaneously hypertensive rats. Our recent studies show that nNOS expression in the gracile nucleus is enhanced by low frequency EA applied to the hindlimb acupoints in rats accompanied by increase nNOS protein level. Preliminary results demonstrate that microinjection of either a nitric oxide (NO) donor or L-arginine into the gracile nucleus alters cardiovascular responses to EA stimulation of the acupoints. Spinothalamic tract cells located in the gracile nucleus are activated by a single electrical stimulus to the sciatic nerve while synaptic transmission through the dorsal column is depressed by a gamma-aminobutyric acid (GABA)-mediated depolarization of the gracile afferents. The purpose of the proposed research is to study our hypotheses that EA stimulation of hindlimb acupoints induces up-regulation of nNOS expression in the gracile nucleus, and the nNOS-NO-GABA system acts as an inhibitory modulation of cardiovascular functions in the gracile-thalamic pathways. The major aims are to determine: 1) Does NO in the gracile nucleus modify the sympatho- and cardiovascular responses to EA applied to the hindlimb acupoints? 2) Does GABAergic transmission mediate the inhibitory responses of NO on EA stimulation in the gracile nucleus? 3) Do time- and concentration-responses to EA-induced endogenous NO release in the gracile nucleus parallel the sympatho- and cardiovascular responses? 4) Is nNOS expression in the gracile nucleus selectively up-regulated by the EA? And 5) What are the distributions of Fos/nNOS expression in the gracile-thalamic pathways induced by the EA? The physiological recordings of arterial blood pressure, heart rate, and renal sympathetic nerve activity will incorporate with EA stimulation and neuropharmacological manipulations and histochemical studies to test the hypotheses in rat models. The results should advance our understanding of the sites and influences of low-frequency EA applied to the hindlimb acupoints on nNOS regulation in the gracile nucleus, and yield new insights regarding central mechanisms of NO and EA on sympathoinhibition.