Schwartz G J
Edward W. Bourne Behavioral Research Laboratory, Weill Medical College of Cornell University, White Plains, New York, USA.
Nutrition. 2000 Oct;16(10):866-73. doi: 10.1016/s0899-9007(00)00464-0.
Meals are the functional units of food intake in humans and mammals, and physiologic approaches to understanding the controls of meal size have demonstrated that the presence of food in the upper gastrointestinal tract plays a critical role in determining meal size. The vagus nerve is the primary neuroanatomic substrate in the gut-brain axis, transmitting meal-related signals elicited by nutrient contact with the gastrointestinal tract to sites in the central nervous system that mediate ingestive behavior. This article describes progress in examining the role of the vagal gut-brain axis in the negative-feedback control of meal size from four perspectives: neuroanatomic, neurophysiologic, molecular, and behavioral. Vagal afferents are strategically localized to be sensitive to meal-related stimuli, and their central projections are organized viscerotopically in the caudal brainstem. Vagal afferents are sensitive to mechanical, chemical, and gut and peptide meal-related stimuli and can integrate multiple such modalities. Meal-elicited gastrointestinal stimuli activate distinct patterns of c-fos neural activation within caudal brainstem sites, where gut vagal afferents terminate. Results of selective chemical and surgical vagal deafferentation studies have refined our understanding of the sites and types of critical gastrointestinal feedback signals in the control of meal size. Recent behavioral, molecular, and neurophysiologic data have demonstrated brainstem sites where centrally acting neuropeptides may modulate the processing of gut vagal afferent meal-related signals to alter feeding. Investigations of the structure and function of splanchnic visceral afferents and enterics and characterization of the integrative capacities of the hindbrain and forebrain components of the gut-brain axis are critical next steps in this analysis.
进餐是人类和哺乳动物摄入食物的功能单位，从生理学角度理解进餐量的控制表明，上消化道中食物的存在对确定进餐量起着关键作用。迷走神经是肠-脑轴中的主要神经解剖学基础，它将胃肠道与营养物质接触引发的与进餐相关的信号传递到中枢神经系统中调节摄食行为的部位。本文从神经解剖学、神经生理学、分子学和行为学四个角度描述了研究迷走神经肠-脑轴在进餐量负反馈控制中作用的进展。迷走神经传入纤维在战略上定位为对与进餐相关的刺激敏感，其向中枢的投射在延髓尾部按内脏部位进行组织。迷走神经传入纤维对机械、化学以及与肠道和肽类进餐相关的刺激敏感，并且能够整合多种此类刺激方式。进餐引发的胃肠道刺激激活了延髓尾部迷走神经传入纤维终止部位内不同模式的c-fos神经激活。选择性化学和手术切断迷走神经传入纤维的研究结果，使我们对控制进餐量时关键胃肠道反馈信号的部位和类型有了更深入的了解。最近的行为学、分子学和神经生理学数据表明，脑干部位存在一些中枢作用的神经肽，它们可能调节肠道迷走神经传入纤维与进餐相关信号的处理过程，从而改变进食行为。对内脏内脏传入纤维和肠神经系统的结构与功能进行研究，以及对肠-脑轴的后脑和前脑成分的整合能力进行表征，是该分析接下来的关键步骤。
