BRAINSTEM ESOPHAGEAL - GASTRIC CONTROL REFLEXES

食道扩张-胃松弛反应或“接受性松弛反射”[RRR]是一种自主神经机制，通常会增加胃容量，降低胃内压，以确保吞咽的食物有效地输送到胃并保留在胃中。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的存在。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。这种反射机制的失效被认为是一些严重的吞咽和反流障碍的原因。这种产生胃松弛的回路也可能在恶心的感觉和呕吐的产生中发挥关键作用。我们的初步结果表明，食道迷走神经的中央RR回路与孤束核中央部分(NSTc)有联系，NSTc进而投射到整个迷走神经背侧运动核[DMN]。DMN传出神经控制胃的运动和顺应性功能，可分为两条不同的迷走神经通路。另一个DMN投射到胃可能激活了一个非肾上腺素能非胆碱能[NaNC]肠路。根据我们的初步生理数据，我们提出了以下假设：由食道传入激活的NSTc神经元工作在通往胃的这两条不同的DMN通路上，因此毒扁豆碱[兴奋]通路被抑制，而NaNC[抑制]通路被激活。这些效果的结合产生了一种深刻的放松。此外，我们预测由心理应激激活的促肾上腺皮质激素释放激素[CRH]能中枢神经系统机制可能通过激活迷走神经背侧复合体中的RR环路元件而导致胃淤滞。这些预测将通过体内和体外神经生理学和免疫细胞化学方案的组合进行验证。

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.