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A Distinct Subpopulation of Extended Amygdala Neurons Drives Food Intake.

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Updated: Jan 10, 2026

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A Distinct Subpopulation of Extended Amygdala Neurons Drives Food Intake.

Isaac F Kandil1, Ethan T Rogers1, Allison R Morningstar1

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Vasoactive intestinal peptide receptor 2 (Vipr2) neurons in the oval bed nucleus of the stria terminalis promote feeding. Food restriction activates these neurons, which project to hypothalamic feeding centers.

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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 ovBNST neuronal subpopulations contributing to feeding regulation remain poorly understood.

Purpose of the Study:

  • To investigate the role of vasoactive intestinal peptide receptor 2 (Vipr2) expressing ovBNST neurons in regulating food intake.
  • To elucidate the neural circuits and upstream signals regulating these neurons.

Main Methods:

  • Chemogenetics using DREADDs to activate ovBNST Vipr2 neurons.
  • Immunohistochemistry and cFos activation mapping in Vipr2-tdTomato reporter mice.
  • Viral circuit tracing to identify projections from ovBNST Vipr2 neurons.

Main Results:

  • Chemogenetic activation of ovBNST Vipr2 neurons significantly increased food intake.
  • Food restriction robustly activated ovBNST Vipr2 neurons, associated with decreased VIP innervation.
  • Vipr2 and PKCδ mark distinct ovBNST neuronal populations with opposing effects on feeding.
  • ovBNST Vipr2 neurons project to the parasubthalamic nucleus (PSTN) and paraventricular nucleus of the hypothalamus (PVN).

Conclusions:

  • ovBNST Vipr2 neurons are a distinct subpopulation that promotes feeding.
  • These neurons are activated by food restriction and link BNST neuropeptide signaling to hypothalamic feeding centers.