Abstract:
: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.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Wang Y,Kim J,Schmit MB,Cho TS,Fang C,Cai Hdoi
10.1038/s41467-019-10715-xsubject
Has Abstractpub_date
2019-06-24 00:00:00pages
2769issue
1issn
2041-1723pii
10.1038/s41467-019-10715-xjournal_volume
10pub_type
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