| 段秋霞,栾 晓,郭菲菲,孙向荣,徐 珞.大鼠ARC-BMA nesfatin-1神经通路及对GD神经元放电活动和胃运动的影响[J].,2017,17(27):5227-5232 |
| 大鼠ARC-BMA nesfatin-1神经通路及对GD神经元放电活动和胃运动的影响 |
| Nesfatin-1 Signaling in the Basom Edial Amygdala Modulates the Gastric Distension-sensitive Neurons Discharge and Decreases Gastric Motility by the Arcuate Nucleus |
| 投稿时间：2017-03-25 修订日期：2017-04-21 |
| DOI：10.13241/j.cnki.pmb.2017.27.007 |
| 中文关键词: Nesfatin-1 杏仁核 弓状核 胃牵张敏感神经元 胃运动 |
| 英文关键词: Nesfatin-1 Amygdala Arcuate nucleus Gastric distension responsive neurons Gastric motility |
| 基金项目:国家自然科学基金项目（81470815,81270460,81500414）；山东省优秀中青年科学基金项目（BS2014YY009）；青岛市科技局项目（14-2-3-3-nsh） |
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| 中文摘要: |
| 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: |
| ABSTRACT 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 ampli- tude 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, P＜0.01） and decreased the firing rate of most of the GD-I neurons（3.73±0.92 Hz vs. 2.64±0.86 Hz， P＜0.01）, 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, P＜0.05; GD-I: 2.84±0.86 Hz vs. 4.05±1.12 Hz, P＜0.05） 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. |
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