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Combining Quantitative Food-intake Assays and Forcibly Activating Neurons to Study Appetite in Drosophila

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Published on: April 24, 2018

Deciphering a neuronal circuit that mediates appetite.

Qi Wu¹, Michael S Clark, Richard D Palmiter

¹Howard Hughes Medical Institute and Department of Biochemistry, University of Washington School of Medicine, Seattle, Washington 98195, USA.

|March 16, 2012

Summary

This summary is machine-generated.

Ablating agouti-related protein (AgRP) neurons causes starvation by exciting the parabrachial nucleus (PBN). Glutamatergic NTS and serotonergic neurons drive this PBN excitation, controlling feeding and body weight.

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Area of Science:

Neuroscience
Neurobiology
Physiology

Background:

Agouti-related protein (AgRP) neurons in the hypothalamus promote feeding and weight gain.
Ablation of AgRP neurons leads to starvation, linked to parabrachial nucleus (PBN) overactivation.
The source of excitatory input to the PBN driving this starvation response was previously unknown.

Purpose of the Study:

To identify the neural circuits responsible for PBN excitation following AgRP neuron ablation.
To elucidate the role of specific neuronal populations in modulating feeding behavior and body weight.
To investigate the PBN as a central hub for integrating feeding-related signals.

Main Methods:

Utilized mouse models with targeted genetic manipulations and pharmacological interventions.
Investigated the role of glutamatergic neurons in the nucleus tractus solitarius (NTS) and serotonergic neurons.
Examined the effects of manipulating serotonin (5-HT3) receptors and N-methyl D-aspartate (NMDA) receptors in the PBN.

Main Results:

Glutamatergic NTS neurons and caudal serotonergic neurons excite PBN neurons, inhibiting feeding.
Blocking serotonin (5-HT3) receptor signaling in the NTS or inactivating Tph2 in serotonergic neurons prevents starvation after AgRP neuron ablation.
Inactivating NTS glutamatergic signaling to PBN NMDA receptors also prevents starvation.
Suppressing PBN glutamatergic output reinstates appetite after AgRP neuron ablation and promotes weight gain otherwise.

Conclusions:

Identified glutamatergic NTS and serotonergic neurons as key drivers of PBN excitation and feeding inhibition.
The PBN acts as a critical integration hub, receiving inputs that bidirectionally control feeding and body weight.
This study reveals novel neural pathways regulating appetite and energy balance.