TrkB-expressing paraventricular hypothalamic neurons suppress appetite through multiple neurocircuits

Juan Ji An, Clint E. Kinney, Ji-Wei Tan, Guey-Ying Liao, Eric J. Kremer and Baoji Xu ()
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Juan Ji An: The Scripps Research Institute Florida
Clint E. Kinney: The Scripps Research Institute Florida
Ji-Wei Tan: The Scripps Research Institute Florida
Guey-Ying Liao: The Scripps Research Institute Florida
Eric J. Kremer: University of Montpellier, CNRS
Baoji Xu: The Scripps Research Institute Florida

Nature Communications, 2020, vol. 11, issue 1, 1-16

Abstract: 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 (PVHTrkB) neurons suppresses or increases food intake, respectively. PVHTrkB neurons project to multiple brain regions, including ventromedial hypothalamus (VMH) and lateral parabrachial nucleus (LPBN). We find that PVHTrkB neurons projecting to LPBN are distinct from those to VMH, yet Ntrk2 deletion in PVH neurons projecting to either VMH or LPBN results in hyperphagia and obesity. Additionally, TrkB activation with BDNF increases firing of these PVH neurons. Therefore, TrkB signaling is a key regulator of a previously uncharacterized neuronal population within the PVH that impinges upon multiple circuits to govern appetite.

Date: 2020
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DOI: 10.1038/s41467-020-15537-w

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