Energy state guides reward seeking via an extended amygdala to lateral hypothalamus pathway

Kuldeep Shrivastava, Vikshar Athreya, Yi Lu, Jorge Luis-Islas, Ashley Han, Tess F. Kowalski and Mark A. Rossi ()
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Kuldeep Shrivastava: Rutgers Robert Wood Johnson Medical School
Vikshar Athreya: Rutgers Robert Wood Johnson Medical School
Yi Lu: Rutgers Robert Wood Johnson Medical School
Jorge Luis-Islas: Rutgers Robert Wood Johnson Medical School
Ashley Han: Rutgers Robert Wood Johnson Medical School
Tess F. Kowalski: Rutgers Robert Wood Johnson Medical School
Mark A. Rossi: Rutgers Robert Wood Johnson Medical School

Nature Communications, 2025, vol. 16, issue 1, 1-16

Abstract: Abstract Impaired regulation of food intake underlies numerous health problems, including obesity and type 2 diabetes, yet how brain systems controlling reward seeking become dysregulated to promote overeating is unknown. Glutamatergic neurons of the lateral hypothalamic area (LHA) are thought to act as a brake on feeding, which is dysregulated during diet-induced obesity. These neurons receive input from the extended amygdala, including the bed nucleus of the stria terminalis (BNST). However, the circuit mechanisms underlying the ability of this pathway to control feeding behavior and how they contribute to dysregulated eating are unclear. Here, we discover that BNST projections to LHA (BNST→LHA) promote reward seeking in an energy state-dependent manner by combining optogenetics, in vivo multiphoton calcium imaging, and electrophysiology in mice. Synaptic strength and neuronal function within the BNST→LHA pathway are dynamically regulated according to energy state to guide reward seeking. These findings suggest that hormonal factors modulate the function of the BNST→LHA pathway to align food seeking with current energy needs.

Date: 2025
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DOI: 10.1038/s41467-025-59686-2

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