期刊
CELL REPORTS
卷 12, 期 5, 页码 726-733出版社
CELL PRESS
DOI: 10.1016/j.celrep.2015.06.062
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资金
- Sinsheimer Scholar Foundation
- NJ Health Foundation
- US-Israel Binational Science Foundation (BSF)
- Robert Wood Johnson Foundation
- NIH grant [DA035594]
Glucagon-likepeptide-1 (GLP-1) andits analogs act as appetite suppressants and have been proven to be clinically efficacious in reducing body weight in obese individuals. Central GLP-1 is expressed in a small population of brainstem cells located in the nucleus tractus solitarius (NTS), which project to a wide range of brain areas. However, it remains unclear how endogenous GLP-1 released in the brain contributes to appetite regulation. Using chemogenetic tools, we discovered that central GLP-1 acts on the midbrain ventral tegmental area (VTA) and suppresses high-fat food intake. We used integrated pathway tracing and synaptic physiology to further demonstrate that activation of GLP-1 receptors specifically reduces the excitatory synaptic strength of dopamine (DA) neurons within the VTA that project to the nucleus accumbens (NAc) medial shell. These data suggest that GLP-1 released from NTS neurons can reduce highly palatable food intake by suppressing mesolimbic DA signaling.
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