Department of Neuroscience, University of Arizona, Tucson, AZ, 85721, USA.
Department of Physiology and Pathophysiology, Xi'an Jiaotong University Health Science Center, Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education, Xi'an, 710061, P.R. China.
Nat Commun. 2019 Jun 24;10(1):2769. doi: 10.1038/s41467-019-10715-x.
Loss of appetite or anorexia associated with inflammation impairs quality of life and increases morbidity in many diseases. However, the exact neural mechanism that mediates inflammation-associated anorexia is still poorly understood. Here we identified a population of neurons, marked by the expression of protein kinase C-delta, in the oval region of the bed nucleus of the stria terminalis (BNST), which are activated by various inflammatory signals. Silencing of these neurons attenuates the anorexia caused by these inflammatory signals. Our results demonstrate that these neurons mediate bidirectional control of general feeding behaviors. These neurons inhibit the lateral hypothalamus-projecting neurons in the ventrolateral part of BNST to regulate feeding, receive inputs from the canonical feeding regions of arcuate nucleus and parabrachial nucleus. Our data therefore define a BNST microcircuit that might coordinate canonical feeding centers to regulate food intake, which could offer therapeutic targets for feeding-related diseases such as anorexia and obesity.
与炎症相关的食欲不振或厌食会降低许多疾病的生活质量并增加发病率。然而，介导炎症相关厌食的确切神经机制仍知之甚少。在这里，我们鉴定了终纹床核（BNST）卵圆区中表达蛋白激酶 C-δ的神经元群体，这些神经元被各种炎症信号激活。沉默这些神经元可减轻这些炎症信号引起的厌食。我们的结果表明，这些神经元介导了一般摄食行为的双向控制。这些神经元抑制 BNST 腹外侧部投射到外侧下丘脑的神经元以调节摄食，接收来自弓状核和臂旁核经典摄食区的输入。因此，我们的数据定义了一个 BNST 微电路，它可能协调经典摄食中枢来调节食物摄入，这可能为摄食相关疾病（如厌食症和肥胖症）提供治疗靶点。
