Bieger D
Faculty of Medicine, Memorial University of Newfoundland, St. John's, Canada.
Dysphagia. 1993;8(3):203-8. doi: 10.1007/BF01354539.
The evidence reviewed in this essay supports the following working model of the central function generator for esophageal peristalsis in the rat: solitarial subnucleus centralis (NTSc) neurons operate in a dual capacity as esophagomotor reflex interneurons and as command neurons programming respective outputs from nucleus ambiguus compact formation (AMBc) motoneurons during secondary and primary peristalsis. In both conditions, there is a critical requirement for cholinergic input which enables NTSc neurons to generate the timed sequence of AMBc motoneuronal activity. In primary peristalsis, the cholinergic coupling mechanism is activated centrally, probably via projections from deglutitive premotor neurons to the parvicellular reticular formation and thence to the NTS. In reflex (or secondary) peristalsis, the cholinergic input could in part be generated by cholinergic vagal viscerosensory fibers innervating the esophagus. Postulated connections between NTS deglutitive neurons and the parvicellular cholinergic neurons of the intermediate reticular formation have yet to be demonstrated. Premotor input from NTSc to AMBc is generated by somatostatinergic and excitatory aminoacidergic neurons. Coactivation of both inputs by cholinergic afferents is necessary to generate esophagomotor output from AMBc neurons. The model under study is derived from investigations into central mechanisms governing striated muscle peristaltic activity. Whether the basic operational principles revealed thus far apply to peristaltic pattern generation in species with a smooth muscle esophagus, requires further investigation.
孤束核中央亚核(NTSc)神经元具有双重功能,既是食管运动反射中间神经元,又是在继发性和原发性蠕动过程中对疑核致密部(AMBc)运动神经元的各自输出进行编程的指令神经元。在这两种情况下,胆碱能输入都至关重要,它能使NTSc神经元产生AMBc运动神经元活动的定时序列。在原发性蠕动中,胆碱能耦合机制在中枢被激活,可能是通过吞咽前运动神经元投射到小细胞网状结构,再由此投射到孤束核。在反射性(或继发性)蠕动中,胆碱能输入部分可能由支配食管的胆碱能迷走内脏感觉纤维产生。NTSc吞咽神经元与中间网状结构的小细胞胆碱能神经元之间的假定连接尚未得到证实。NTSc向AMBc的前运动输入由生长抑素能和兴奋性氨基酸能神经元产生。胆碱能传入纤维对这两种输入的共同激活是从AMBc神经元产生食管运动输出所必需的。所研究的模型源自对控制横纹肌蠕动活动的中枢机制的研究。迄今为止所揭示的基本运作原理是否适用于平滑肌食管物种的蠕动模式生成,尚需进一步研究。