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TrkB-expressing paraventricular hypothalamic neurons suppress appetite through multiple neurocircuits
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TrkB-expressing paraventricular hypothalamic neurons suppress appetite through multiple neurocircuits
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Journal Article
TrkB-expressing paraventricular hypothalamic neurons suppress appetite through multiple neurocircuits
2020
Overview
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 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.
The TrkB receptor is known to regulate obesity via appetite control, but the underlying neural circuits are not known. Here, the authors show that selective modulation of TrkB+ neurons in the paraventricular hypothalamus regulates food intake via circuits to ventromedial hypothalamus and lateral parabrachial nucleus.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 38/1
/ 38/32
/ 45/41
/ 64/60
/ Animals
/ Appetite
/ Brain-derived neurotrophic factor
/ Circuits
/ Deletion
/ Endocrinology and metabolism
/ Feeding Behavior - physiology
/ Female
/ Humanities and Social Sciences
/ Membrane Glycoproteins - genetics
/ Membrane Glycoproteins - metabolism
/ Mice
/ Mutation
/ Neurons
/ Obesity
/ Parabrachial Nucleus - cytology
/ Parabrachial Nucleus - metabolism
/ Parabrachial Nucleus - physiopathology
/ Paraventricular Hypothalamic Nucleus
/ Paraventricular Hypothalamic Nucleus - cytology
/ Paraventricular Hypothalamic Nucleus - metabolism
/ Protein-Tyrosine Kinases - genetics
/ Protein-Tyrosine Kinases - metabolism
/ Science
/ Ventromedial Hypothalamic Nucleus
