Autonomic Medicine Section, Clinical Neurosciences Program, Division of Intramural Research, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA; Autonomic Medicine Section, CNP/DIR/NINDS/NIH, 9000 Rockville Pike MSC-1620, Building 10 Room 8N260, Bethesda, MD 20892-1620, USA..
Auton Neurosci. 2021 Dec;236:102889. doi: 10.1016/j.autneu.2021.102889. Epub 2021 Oct 2.
This review updates three key concepts of autonomic neuroscience-stress, the autonomic nervous system (ANS), and homeostasis. Hans Selye popularized stress as a scientific idea. He defined stress variously as a stereotyped response pattern, a state that evokes this pattern, or a stimulus that evokes the state. According to the "homeostat" theory stress is a condition where a comparator senses a discrepancy between sensed afferent input and a response algorithm, the integrated error signal eliciting specific patterns of altered effector outflows. Scientific advances since Langley's definition of the ANS have incited the proposal here of the "extended autonomic system," or EAS, for three reasons. (1) Several neuroendocrine systems are bound inextricably to Langley's ANS. The first to be described, by Cannon in the early 1900s, involves the hormone adrenaline, the main effector chemical of the sympathetic adrenergic system. Other neuroendocrine systems are the hypothalamic-pituitary-adrenocortical system, the arginine vasopressin system, and the renin-angiotensin-aldosterone system. (2) An evolving body of research links the ANS complexly with inflammatory/immune systems, including vagal anti-inflammatory and catecholamine-related inflammasomal components. (3) A hierarchical network of brain centers (the central autonomic network, CAN) regulates ANS outflows. Embedded within the CAN is the central stress system conceptualized by Chrousos and Gold. According to the allostasis concept, homeostatic input-output curves can be altered in an anticipatory, feed-forward manner; and prolonged or inappropriate allostatic adjustments increase wear-and-tear (allostatic load), resulting in chronic, stress-related, multi-system disorders. This review concludes with sections on clinical and therapeutic implications of the updated concepts offered here.
这篇综述更新了自主神经科学的三个关键概念——应激、自主神经系统 (ANS) 和内稳态。汉斯·塞尔耶 (Hans Selye) 将应激作为一个科学概念普及开来。他将应激定义为刻板的反应模式、引起这种模式的状态，或引起这种状态的刺激。根据“内稳态”理论，应激是一种比较器感知传入输入与反应算法之间差异的状态，综合误差信号引发特定的效应器输出改变模式。自兰利 (Langley) 定义 ANS 以来的科学进展促使人们提出了“扩展自主系统”(EAS)，原因有三。(1) 几个神经内分泌系统与兰利的 ANS 紧密结合。第一个由坎农 (Cannon) 在 20 世纪初描述，涉及激素肾上腺素，这是交感肾上腺素能系统的主要效应化学物质。其他神经内分泌系统包括下丘脑-垂体-肾上腺皮质系统、精氨酸加压素系统和肾素-血管紧张素-醛固酮系统。(2) 越来越多的研究将 ANS 与炎症/免疫系统复杂地联系在一起，包括迷走神经抗炎和儿茶酚胺相关的炎症小体成分。(3) 大脑中枢的分层网络（中枢自主网络，CAN）调节 ANS 的输出。中央应激系统嵌入在 CAN 中，由 Chrousos 和 Gold 提出。根据适应的概念，内稳态的输入-输出曲线可以以预期的、前馈的方式改变；而长期或不适当的适应调节会增加磨损（适应负荷），导致慢性、应激相关的多系统疾病。这篇综述最后介绍了这里提供的更新概念的临床和治疗意义。
