NPY-mediated synaptic plasticity in the extended amygdala prioritizes feeding during starvation

Stephan Dodt, Noah V. Widdershooven, Marie-Luise Dreisow, Lisa Weiher, Lukas Steuernagel, F. Thomas Wunderlich, Jens C. Brüning () and Henning Fenselau ()
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Stephan Dodt: Max Planck Institute for Metabolism Research
Noah V. Widdershooven: Max Planck Institute for Metabolism Research
Marie-Luise Dreisow: Max Planck Institute for Metabolism Research
Lisa Weiher: Max Planck Institute for Metabolism Research
Lukas Steuernagel: Max Planck Institute for Metabolism Research
F. Thomas Wunderlich: Max Planck Institute for Metabolism Research
Jens C. Brüning: Max Planck Institute for Metabolism Research
Henning Fenselau: Max Planck Institute for Metabolism Research

Nature Communications, 2024, vol. 15, issue 1, 1-16

Abstract: Abstract Efficient control of feeding behavior requires the coordinated adjustment of complex motivational and affective neurocircuits. Neuropeptides from energy-sensing hypothalamic neurons are potent feeding modulators, but how these endogenous signals shape relevant circuits remains unclear. Here, we examine how the orexigenic neuropeptide Y (NPY) adapts GABAergic inputs to the bed nucleus of the stria terminalis (BNST). We find that fasting increases synaptic connectivity between agouti-related peptide (AgRP)-expressing ‘hunger’ and BNST neurons, a circuit that promotes feeding. In contrast, GABAergic input from the central amygdala (CeA), an extended amygdala circuit that decreases feeding, is reduced. Activating NPY-expressing AgRP neurons evokes these synaptic adaptations, which are absent in NPY-deficient mice. Moreover, fasting diminishes the ability of CeA projections in the BNST to suppress food intake, and NPY-deficient mice fail to decrease anxiety in order to promote feeding. Thus, AgRP neurons drive input-specific synaptic plasticity, enabling a selective shift in hunger and anxiety signaling during starvation through NPY.

Date: 2024
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DOI: 10.1038/s41467-024-49766-0

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