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BRAINSTEM ESOPHAGEAL - GASTRIC CONTROL REFLEXES

BRAINSTEM ESOPHAGEAL - GASTRIC CONTROL REFLEXES
脑干食管 - 胃控制反射
批准号:
6661176
负责人:
Richard C. Rogers
金额:
$13.07万
依托单位国家:
美国
项目类别:
财政年份:
1999
资助国家:
美国
项目状态:
已结题
起止时间:
1999-09-01 至 2005-02-28

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中文摘要
翻译
食道扩张-胃松弛反应或“接受性松弛反射”[RRR]是一种自主机制,通常通过增加胃容量和降低胃内压力来确保吞咽的食物被有效地运送到胃并被胃保留。有大量的描述性文献支持RRR在包括老鼠和人类在内的许多物种中存在。这种反射在很大程度上是由迷走神经传入-中枢-迷走神经传出通路介导的。这种反射机制的失败被认为是导致许多严重的吞咽和反流疾病的原因。这种产生胃松弛的神经回路也可能在恶心的感觉和呕吐的产生中起关键作用。我们的初步结果表明,食道迷走神经传入的中央RR回路与孤立束核中央部(NSTc)相连,而中央部又投射到整个迷走神经背侧运动核[DMN]。控制胃运动和顺应功能的DMN传出可分为两个不同的迷走神经通路。另一个DMN投射到胃可能激活非肾上腺素能非胆碱能[NANC]肠回路。根据我们初步的生理数据,我们提出了以下假设:被食道传入输入激活的NSTc神经元作用于这两条通往胃的DMN通路,使得毒碱(“兴奋”)通路被抑制,而NANC(“抑制”)通路被激活。这些作用的结合产生了一种深刻的放松。此外,我们预测先前发现的促肾上腺皮质激素释放激素[CRH]-由心理应激激活的中枢神经系统机制通过激活迷走背复核中的RR回路元件产生胃停滞。这些预测将通过体内和体外神经生理和免疫细胞化学方案的组合进行测试。
英文摘要
The esophageal distension-gastric relaxation response or "receptive relaxation reflex" [RRR] is an autonomic mechanism which normally increases gastric volume and reduces intragastric pressure to assure that swallowed food is efficiently transported to and retained by the stomach. There is a large body of descriptive literature which supports the existence of the RRR in a number of species including rats and humans. This reflex is mediated largely, is not exclusively by a vagal afferent-CNS-vagal efferent pathway. Failure of this reflex mechanism has been held responsible for a number of serious swallowing and reflux disorders. This circuitry, which produces gastric relaxation, may also play a critical role in the perception of nausea and the production of emesis. Our preliminary results suggest that the central RR circuitry of esophageal vagal afferent connections with the nucleus of the solitary tract, pars centralis (NSTc] which, in turn, projects throughout the entire dorsal motor nucleus of the vagus [DMN]. DMN efferents which control the motility and compliance functions of the stomach are separable into two distinct vagal pathway. The other DMN projection to the stomach probably activates a non-adrenergic non-cholinergic [NANC] enteric circuit. Based on our preliminary physiological data we formulate the following hypotheses: the NSTc neurons activated by esophageal afferent input operate on these two separate DMN pathways to the stomach such that the muscarinic ["excitatory"] pathway is inhibited while the NANC ["inhibitory"] pathway is activated. The combination of effects produces a profound relaxation. Furthermore, we predict that a previously identified corticotrophin releasing hormone [CRH]- ergic CNS mechanism activated by psychological stress produces gastric stasis by activating RR circuit elements in the dorsal vagal complex. These predictions will be tested by a combination of in vivo and in vitro neurophysiological and immunocytochemical protocols.
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