Abstract：
:To understand hindbrain pathways involved in the control of food intake, we examined roles for calcitonin receptor (CALCR)-containing neurons in the NTS. Ablation of NTS Calcr abrogated the long-term suppression of food intake, but not aversive responses, by CALCR agonists. Similarly, activating CalcrNTS neurons decreased food intake and body weight but (unlike neighboring CckNTS cells) failed to promote aversion, revealing that CalcrNTS neurons mediate a non-aversive suppression of food intake. While both CalcrNTS and CckNTS neurons decreased feeding via projections to the PBN, CckNTS cells activated aversive CGRPPBN cells while CalcrNTS cells activated distinct non-CGRP PBN cells. Hence, CalcrNTS cells suppress feeding via non-aversive, non-CGRP PBN targets. Additionally, silencing CalcrNTS cells blunted food intake suppression by gut peptides and nutrients, increasing food intake and promoting obesity. Hence, CalcrNTS neurons define a hindbrain system that participates in physiological energy balance and suppresses food intake without activating aversive systems.
journal_name
Cell Metabjournal_title
Cell metabolismauthors
Cheng W,Gonzalez I,Pan W,Tsang AH,Adams J,Ndoka E,Gordian D,Khoury B,Roelofs K,Evers SS,MacKinnon A,Wu S,Frikke-Schmidt H,Flak JN,Trevaskis JL,Rhodes CJ,Fukada SI,Seeley RJ,Sandoval DA,Olson DP,Blouet C,Myers MGdoi
10.1016/j.cmet.2019.12.012subject
Has Abstractpub_date
2020-02-04 00:00:00pages
301-312.e5issue
2eissn
1550-4131issn
1932-7420pii
S1550-4131(19)30677-1journal_volume
31pub_type
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