TrkB-expressing paraventricular hypothalamic neurons suppress appetite through multiple neurocircuits.

ABSTRACT: The TrkB receptor is critical for the control of energy balance, as mutations in its gene (NTRK2) lead to hyperphagia and severe obesity. The main neural substrate mediating the appetite-suppressing activity of TrkB, however, remains unknown. Here, we demonstrate that selective Ntrk2 deletion within paraventricular hypothalamus (PVH) leads to severe hyperphagic obesity. Furthermore, chemogenetic activation or inhibition of TrkB-expressing PVH (PVH^TrkB) neurons suppresses or increases food intake, respectively. PVH^TrkB neurons project to multiple brain regions, including ventromedial hypothalamus (VMH) and lateral parabrachial nucleus (LPBN). We find that PVH^TrkB neurons projecting to LPBN are distinct from those to VMH, yet Ntrk2 deletion in PVH neurons pro

SUBMITTER: An JJ 

PROVIDER: S-EPMC7138837 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature