A bed nucleus of stria terminalis microcircuit regulating inflammation-associated modulation of feeding (Nature Communications 2019, 10:2769)

報告日期: 2020/04/24
報告時間: 16:00/16:50
報告學生: 劉嘉瑋(英文報告)
講評老師: 郭余民
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A bed nucleus of stria terminalis microcircuit regulating inflammation-associated modulation of feeding
Wang et al., 2019, Nat Communications
Speaker: Chia-Wei Liou;  Commentator: Yu-Min Kuo, Ph.D.

Inflammation-associated anorexia or loss of appetite during acute diseases can restrict the intake of nutrients to inhibit bacterial growth and eliminate pathogens [1]. However, inflammation-associated anorexia during chronic disease leads to negative effects on recovery and increase morbidity [1]. Intraperitoneal (i.p.) injection of pro-inflammatory cytokines, e.g. interleukin-1β (IL-1β) and stimulants, e.g. lipopolysaccharides (LPS) have been demonstrated in animal studies and decreased food intake of mice [2, 3]. However, the neural circuit mechanism that modulate inflammation-associated anorexia is still unclear. The authors identified a population of neurons, highly expressed protein kinase C-delta (PKC-δ), in oval part of the bed nucleus of the stria terminalis (ovBNST) which are activated by i.p. IL-1β and LPS injection. They hypothesized that the PKC-δ neurons in ovBNST regulate inflammation-associated anorexia. Inhibition of ovBNST PKC-δ neurons by chemogenetics approach aleviated anorexia caused by IL-1β and LPS peripheral administration. Activation of ovBNST PKC-δ neurons by optogenetics approach decreased food intake of mice indicating these neurons can regulate feeding behavior. The authors also observed that ovBNST PKC-δ neurons inhibit ventrolateral BNST to lateral hypothalamus circuit which have antagonized effect of ovBNST PKC-δ neurons activation to regulate food intake. Furthermore, injection of monosynaptic retrograde rabies virus specific in ovBNST PKC-δ neurons showed multiple canonical feeding-related brain regions, e.g. arcuate nucleus (ARC) and lateral parabrachial nucleus (LPB) sent inputs to ovBNST PKC-δ neurons. These results suggested ovBNST PKC-δ neurons may integrate feeding signals to modulate food intake of mice. Thus, this paper identified a unique neuron population and demonstrated the microcircuit in BNST to regulate inflammation-associated anorexia and feeding behavior.   

Reference:

  1. Plata-Salaman, C.R., Anorexia during acute and chronic disease. Nutrition, 1996. 12(2): p. 69-78.
  2. Langhans, W., D. Savoldelli, and S. Weingarten, Comparison of the feeding responses to bacterial lipopolysaccharide and interleukin-1 beta. Physiol Behav, 1993. 53(4): p. 643-9.
  3. Kent, S., et al., Mechanisms of sickness-induced decreases in food-motivated behavior. Neurosci Biobehav Rev, 1996. 20(1): p. 171-5.