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Trk B signaling in dopamine 1 receptor neurons regulates food intake and body weight
Author(s) -
Mason Brittany L.,
Lobo Mary Kay,
Parada Luis F.,
Lutter Michael
Publication year - 2013
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1002/oby.20382
Subject(s) - dopamine , trk receptor , receptor , dopamine receptor , body weight , food intake , endocrinology , medicine , neuroscience , chemistry , biology , neurotrophin
Objective Loss of BDNF‐TrkB signaling results in obesity in both humans and mice; however, the neural circuit that mediates this effect is unknown. The role of TrkB signaling in dopamine‐1 receptor expressing neurons in body weight regulation was tested. Methods Mice with a floxed allele of the TrkB gene were paired with mice expressing Cre‐recombinase under control of the D1 promoter to conditionally knock out expression of TrkB receptors from D1‐neurons. Results Deletion of TrkB receptors from D1 neurons results in obesity in chow fed mice due to increased feed efficiency. In contrast, loss of Trk B signaling in D1 neurons induced hyperphagia and hyperglycemia in mice maintained on high fat diet. Conclusions These findings indicate TrkB signaling in D1 neurons regulates body weight by distinct mechanisms for chow and high fat diet and may be important for defending the body against the development of obesity and obesity‐related disorders.