Author:
Sun Runan,Tsunekawa Taku,Hirose Tomonori,Yaginuma Hiroshi,Taki Keigo,Mizoguchi Akira,Miyata Takashi,Kobayashi Tomoko,Sugiyama Mariko,Onoue Takeshi,Takagi Hiroshi,Hagiwara Daisuke,Ito Yoshihiro,Iwama Shintaro,Suga Hidetaka,Banno Ryoichi,Bettler Bernhard,Arima Hiroshi
Abstract
AbstractPrevious studies suggest that signaling by the gamma-aminobutyric acid (GABA) type B receptor (GABABR) is involved in the regulation of binge eating, a disorder which might contribute to the development of obesity. Here, we show that intermittent access to a high fat diet (HFD) induced binge-like eating behavior with activation of dopamine receptor d1 (drd1)-expressing neurons in the caudate putamen (CPu) and nucleus accumbens (NAc) in wild-type (WT) mice. The activation of drd1-expressing neurons during binge-like eating was substantially increased in the CPu, but not in the NAc, in corticostriatal neuron-specific GABABR-deficient knockout (KO) mice compared to WT mice. Treatment with the GABABR agonist, baclofen, suppressed binge-like eating behavior in WT mice, but not in KO mice, as reported previously. Baclofen also suppressed the activation of drd1-expressing neurons in the CPu, but not in the NAc, during binge-like eating in WT mice. Thus, our data suggest that GABABR signaling in CPu neurons expressing drd1 suppresses binge-like consumption during a HFD in mice.
Funder
Japanese Society for Promotion of Science
a Junior Scientist Development Grant supported by Novo Nordisk Pharma Ltd. from the Japan Diabetes Society
the Suzuken Memorial Foundation
Swiss National Science Foundation
Publisher
Springer Science and Business Media LLC
Cited by
4 articles.
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