中文摘要：

目的：探讨弓状核（ARC）-杏仁核（BMA）间nesfatin-1神经通路的构成及其对胃牵张敏感（GD）神经放电活动和胃运动的影响。方法：逆行追踪结合免疫组化观察ARC-BMA间nesfatin-1神经通路;细胞外放电记录,观察nesfatin-1对GD神经元放电活动的影响及电刺激ARC对BMA内GD神经元放电活动的影响;在体胃运动研究,观察nesfatin-1对胃运动及胃排空的影响及电刺激ARC对胃运动的影响。结果：大鼠ARC-BMA间存在nesfatin-1神经通路;BMA微量注射Nesfatin-1能够促进GD-E神经元放电（4.25±1.02 Hz vs.5.32±1.17 Hz,P〈0.01）,抑制GD-I神经元放电（3.73±0.92 Hz vs.2.64±0.86 Hz,P〈0.01）,并且胃收缩频率及幅度下降,nesfatin-1的这些效应可被SHU9119部分阻断;电刺激ARC后,BMA内nesfatin-1反应性GD神经元放电频率增加（GD-E：5.14±1.32 Hz vs.6.75±1.84 Hz,P〈0.05;GD-I：2.84±0.86 Hz vs.4.05±1.12 Hz,P〈0.05）,并且胃收缩频率和幅度增强。结论：ARC-BMA间nesfafin-1通路可调控大鼠胃牵张敏感神经元放电活动和胃运动,该效应可能与黑色素信号通路有关。

英文摘要：

Objective：This study aimed to explore the effects of nesfatin-1 on gastric distension（GD）-sensitive neurons in the basomedial amygdala（BMA） and the potential mechanism for nesfatin-1 to regulate gastric motility through the arcuate nucleus（Arc）.Methods：The projection of nerve fiber and expression of nesfatin-1 were observed by retrograde tracing and fluo-immunohistochemistry staining;The nuclei microinjection and nuclei electrical stimulation,extracellular discharges of single unit neuron were used to observe the effects of nesfatin-1 on the GD neurons;Gastric motility recording in vivo were used to monitor the effects of nesfatin-1 on the amplitude of constriction and frequency of gastric motility in conscious rats.Results：NUCB2/Nesfatin-1/fluorogold-double labeled neurons were from ARC to BMA;Nesfatin-1 could excited the firing rate of most of the GD-E neurons（4.25±1.02 Hz vs.5.32±1.17 Hz,P0.01）and decreased the firing rate of most of the GD-I neurons（3.73±0.92 Hz vs.2.64±0.86 Hz,P0.01）,inhibited the gastric motility,amplitude and frequency,SHU9119 could weaken the responses induced by nesfaton-1;Electrical stimulation of the Arc,the firing rate of nesfatin-1-induced GD-response neurons（GD-E：5.14±1.32 Hz vs.6.75±1.84 Hz,P0.05;GD-I：2.84±0.86 Hz vs.4.05±1.12 Hz,P0.05）and the gastric amplitude and frequency were increase.Conclusion：It was suggested that nesfatin-1 in the BMA plays an important role in decreasing gastric motility and the Arc may be involved in this regulation process.