BRAINSTEM ESOPHAGEAL - GASTRIC CONTROL REFLEXES

食管扩张-胃舒张反应或“接受性舒张反射”[RRR]是一种自主机制，其通常增加胃容量并降低胃内压力，以确保吞咽的食物有效地输送到胃并由胃保留。大量描述性文献支持包括大鼠和人类在内的许多种属中存在RRR。这种反射主要是由迷走神经传入-CNS-迷走神经传出通路介导的，而不仅仅是迷走神经传入-CNS-迷走神经传出通路。这种反射机制的失败被认为是造成许多严重的吞咽和反流疾病的原因。这种产生胃松弛的回路也可能在恶心的感知和呕吐的产生中起关键作用。我们的初步结果表明，中央RR回路的食管迷走神经传入连接与孤束核，中央部（NSTc），这反过来，项目在整个背运动核的迷走神经[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投射到胃可能激活非肾上腺素能非胆碱能[NANC]肠道回路。基于我们初步的生理数据，我们提出了以下假设：食管传入输入激活的NSTc神经元对这两个独立的DMN通路进行操作，使毒蕈碱[“兴奋性”]通路被抑制，而NANC [“抑制性”]通路被激活。这些效果的结合产生了深刻的放松。此外，我们预测，以前确定的促肾上腺皮质激素释放激素（CRH）-神经中枢机制激活的心理应激产生胃郁滞激活RR电路元件背迷走神经复合体。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测试。

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.