Department of Physiology and Pathology, School of Dentistry, Universidade Estadual Paulista, Araraquara, São Paulo, Brazil; and Departments of Psychology, Pharmacology and Health, and Human Physiology and the Cardiovascular Center, University of Iowa, Iowa City, Iowa.
Am J Physiol Regul Integr Comp Physiol. 2014 Feb 15;306(4):R201-10. doi: 10.1152/ajpregu.00251.2012. Epub 2014 Jan 8.
In states of sodium deficiency many animals seek and consume salty solutions to restore body fluid homeostasis. These behaviors reflect the presence of sodium appetite that is a manifestation of a pattern of central nervous system (CNS) activity with facilitatory and inhibitory components that are affected by several neurohumoral factors. The primary focus of this review is on one structure in this central system, the lateral parabrachial nucleus (LPBN). However, before turning to a more detailed discussion of the LPBN, a brief overview of body fluid balance-related body-to-brain signaling and the identification of the primary CNS structures and humoral factors involved in the control of sodium appetite is necessary. Angiotensin II, mineralocorticoids, and extracellular osmotic changes act on forebrain areas to facilitate sodium appetite and thirst. In the hindbrain, the LPBN functions as a key integrative node with an ascending output that exerts inhibitory influences on forebrain regions. A nonspecific or general deactivation of LPBN-associated inhibition by GABA or opioid agonists produces NaCl intake in euhydrated rats without any other treatment. Selective LPBN manipulation of other neurotransmitter systems [e.g., serotonin, cholecystokinin (CCK), corticotrophin-releasing factor (CRF), glutamate, ATP, or norepinephrine] greatly enhances NaCl intake when accompanied by additional treatments that induce either thirst or sodium appetite. The LPBN interacts with key forebrain areas that include the subfornical organ and central amygdala to determine sodium intake. To summarize, a model of LPBN inhibitory actions on forebrain facilitatory components for the control of sodium appetite is presented in this review.
在钠缺乏状态下，许多动物会寻找并摄入咸溶液以恢复体液内稳态。这些行为反映了钠食欲的存在，钠食欲是中枢神经系统 (CNS) 活动模式的一种表现，具有促进和抑制成分，受多种神经激素因素的影响。本综述的主要重点是中枢神经系统中的一个结构，即外侧臂旁核 (LPBN)。然而，在更详细地讨论 LPBN 之前，有必要简要概述与体液平衡相关的身体到大脑的信号传递，以及鉴定参与控制钠食欲的主要中枢神经系统结构和激素因素。血管紧张素 II、盐皮质激素和细胞外渗透压变化作用于前脑区域，促进钠食欲和口渴。在后脑，LPBN 作为一个关键的整合节点，具有上行输出，对前脑区域施加抑制影响。GABA 或阿片样激动剂对 LPBN 相关抑制的非特异性或一般失活会导致正常水合的大鼠摄入 NaCl，而无需任何其他治疗。对其他神经递质系统（例如，5-羟色胺、胆囊收缩素 (CCK)、促肾上腺皮质释放因子 (CRF)、谷氨酸、ATP 或去甲肾上腺素）的选择性 LPBN 操作，当伴有诱导口渴或钠食欲的其他治疗时，会极大地增强 NaCl 摄入。LPBN 与关键的前脑区域相互作用，包括穹窿下器官和中央杏仁核，以确定钠的摄入量。总之，本文综述提出了一个关于 LPBN 对控制钠食欲的前脑促进成分的抑制作用的模型。
