Substance P in the lateral hypothalamic area regulates binge-like eating behaviors in mice.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 41802059.
- Also identified by DOI 10.1073/pnas.2524335123 and PMC identifier 12994189.
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Abstract
Binge eating disorder (BED) is the most common type of eating disorder; however, the neural circuit mechanisms underlying BED remain elusive. Here, we report that tachykinin-expressing neurons in the lateral hypothalamic area (LH<sup>Tac1</sup> neurons) are inhibited during binge-like eating behaviors in mice. We identified LH<sup>Tac1</sup> neurons as key mediators of binge-like eating behaviors and reported that the LH<sup>Tac1</sup>→ lateral periaqueductal gray (LPAG) circuit is critical to the regulation of binge-like eating behaviors. Moreover, Substance P (SP) released by LH<sup>Tac1</sup> neurons modulates binge-like eating behaviors by influencing the input of glutamate to LPAG cells, which receive projections from LH<sup>Tac1</sup> neurons. In summary, these findings point to the SP as a key node in BED circuits.
Medical subject headings
- Substance P
- Hypothalamic Area, Lateral
- Feeding Behavior
- Binge-Eating Disorder
- Bulimia