首页> 美国卫生研究院文献>Bioelectronic Medicine >Collateral benefits of studying the vagus nerve in bioelectronic medicine
【2h】

Collateral benefits of studying the vagus nerve in bioelectronic medicine

机译:在生物电子医学中研究迷走神经的附带好处

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

The inflammatory reflex. In the inflammatory reflex, the activity of afferent vagus nerve fibers residing in the nodose ganglion is stimulated by cytokines and pathogen-associated molecular patterns (PAMPs). The signal is transmitted to the NTS. Reciprocal connections between the NTS and DMN mediate communication with and activation of efferent vagus nerve fibers from the DMN. The signal is propagated to the celiac ganglia and the superior mesenteric ganglion in the celiac plexus, where the splenic nerve originates. Norepinephrine (NE) released from the splenic nerve interacts with β -adrenergic receptors (β -ARs) and causes the release of acetylcholine (ACh) from T cells containing functional choline acetyltransferase (T-ChAT cells). ACh interacts with α7nAChRs on macrophages and suppresses proinflammatory cytokine release and inflammation. The inflammatory reflex can be activated through brain mAChR-mediated mechanisms by centrally-acting M1 mAChR agonists and acetylcholinesterase (AChE) inhibitors. Somatosensory activation by electroacupuncture at the Hegu point also causes activation of brain mAChR signaling, which then results in activation of efferent vagus and splenic anti-inflammatory signaling. Electroacupuncture at a different acupuncture point activates sciatic nerve signals, which by unknown mechanisms convert to efferent vagus nerve signaling to the adrenal medulla, resulting in dopamine release. Dopamine suppresses inflammation and improves survival in a model of sepsis. Vagus nerve and splenic nerve signaling mediated through α7nAChR on splenocytes controls inflammation in acute kidney injury and alleviates the condition.
机译:炎症反射。在炎性反射中,细胞因子和病原体相关分子模式(PAMP)刺激了位于结节神经节中的迷走神经传入神经纤维的活动。信号被发送到NTS。 NTS和DMN之间的相互连接介导了与DMN传出的迷走神经纤维的通讯和激活。信号传播到脾神经起源的腹腔神经丛的腹腔神经节和肠系膜上神经节。从脾神经释放的去甲肾上腺素(NE)与β-肾上腺素受体(β-ARs)相互作用,并导致乙酰胆碱(ACh)从含有功能性胆碱乙酰基转移酶的T细胞(T-ChAT细胞)中释放出来。 ACh与巨噬细胞上的α7nAChRs相互作用并抑制促炎细胞因子的释放和炎症。炎症反射可通过脑mAChR介导的机制,由中枢性作用的M1 mAChR激动剂和乙酰胆碱酯酶(AChE)抑制剂激活。通过电针在Hegu点进行体感激活也会导致脑mAChR信号激活,然后导致传出迷走神经激活和脾抗炎信号。在不同的穴位进行电针刺激坐骨神经信号,通过未知机制将其转换为传出的迷走神经信号,传递至肾上腺髓质,导致多巴胺释放。多巴胺在脓毒症模型中抑制炎症并提高生存率。通过α7nAChR介导的脾细胞上的迷走神经和脾神经信号控制了急性肾损伤中的炎症并减轻了病情。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号