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Related Experiment Video

Updated: Jun 16, 2026

Simultaneous Detection of c-Fos Activation from Mesolimbic and Mesocortical Dopamine Reward Sites Following Naive Sugar and Fat Ingestion in Rats

Simultaneous Detection of c-Fos Activation from Mesolimbic and Mesocortical Dopamine Reward Sites Following Naive Sugar and Fat Ingestion in Rats

Published on: August 24, 2016

A Distinct Subpopulation of Extended Amygdala Neurons Drives Food Intake.

Isaac F Kandil¹, Ethan T Rogers¹, Allison R Morningstar¹

¹Wu Tsai Neurosciences Institute and Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, California.

Biological Psychiatry Global Open Science

|June 15, 2026

Summary

Neurons expressing Vipr2 in the oval subnucleus of the bed nucleus of the stria terminalis (ovBNST) promote feeding. These neurons are activated by food restriction and project to hypothalamic feeding centers.

Keywords:

BNST Extended amygdala Feeding Vasoactive intestinal peptide Vipr2

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Area of Science:

Neuroscience
Behavioral Neuroscience
Neuroendocrinology

Background:

The oval subnucleus of the bed nucleus of the stria terminalis (ovBNST) integrates stress and reward signals to regulate motivated behaviors, including feeding.
Specific neuronal subpopulations within the ovBNST and their roles in feeding remain poorly understood.

Purpose of the Study:

To investigate the function of Vipr2-expressing ovBNST neurons in regulating food intake.
To elucidate the neural circuits and neurochemical signaling involved in ovBNST-mediated feeding behaviors.

Main Methods:

Chemogenetics (hM3Dq DREADDs) to activate ovBNST Vipr2 neurons.
Immunohistochemistry and cFos expression to assess neuronal activation and neuropeptide innervation under food restriction.
Viral tracing to map projections of ovBNST Vipr2 neurons.

Main Results:

Chemogenetic activation of ovBNST Vipr2 neurons significantly increased food intake.
Food restriction robustly activated ovBNST Vipr2 neurons and decreased VIP innervation.
Vipr2 and PKCδ mark distinct ovBNST neuronal populations with opposing effects on feeding.
ovBNST Vipr2 neurons project to hypothalamic feeding centers (parasubthalamic and paraventricular nuclei).

Conclusions:

ovBNST Vipr2 neurons represent a distinct subpopulation that promotes feeding.
These neurons are activated by food restriction and link ovBNST signaling to hypothalamic feeding circuits.
This study identifies a novel pathway for regulating motivated feeding behaviors.