Role of the lateral parabrachial nucleus in the control of sodium appetite
Role of the lateral parabrachial nucleus in the control of sodium appetite
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DOI：
10.1152/ajpregu.00251.2012
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发表时间：
2014-02-01
影响因子：
2.8
通讯作者：
Johnson, Alan Kim
中科院分区：
文献类型：
--
作者：
Menani, Jose V.;De Luca, Laurival A., Jr.;Johnson, Alan Kim
在缺钠状态下，许多动物寻求并饮用含盐溶液来恢复体液平衡。这些行为反映了钠摄取的存在，这是中枢神经系统(CNS)活动模式的表现，包括促进和抑制成分，这些成分受到几种神经体液因素的影响。这篇综述的主要焦点是这个中枢系统的一个结构，臂旁外侧核。然而，在对LPBN进行更详细的讨论之前，有必要对与体液平衡相关的体脑信号以及涉及钠摄取控制的主要中枢神经系统结构和体液因素进行简要概述。血管紧张素II、矿物质皮质激素和细胞外渗透变化作用于前脑区域，促进钠的食欲和口渴。在后脑中，LPBN是一个关键的整合节点，其输出呈上升趋势，对前脑区产生抑制作用。GABA或阿片类激动剂对LPBN相关抑制的非特异性或全面性失活可使正常水化大鼠在没有任何其他治疗的情况下摄取氯化钠。选择性的LPBN操作其他神经递质系统[如5-羟色胺、胆囊收缩素(CCK)、促肾上腺皮质激素释放因子(CRF)、谷氨酸、三磷酸腺苷或去甲肾上腺素]，当伴随引起口渴或食欲的额外治疗时，极大地增加了氯化钠的摄入量。LPBN与关键的前脑区域相互作用，包括穹隆下器官和中央杏仁核，以确定钠的摄入量。综上所述，本文综述了LPBN对前脑易化成分的抑制作用模型，以控制钠摄取。
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, mineralo-corticoids, 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.