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Published on: December 16, 2022
Brainstem Astrocytes Regulate Estrus-Dependent Oscillations in Food Intake.
K Selin Ozkaya1, Ceyda Yalcin1, Emily E Haar1
1Department of Neuroscience and Experimental Therapeutics, Penn State University - College of Medicine, Hershey, Pennsylvania, USA.
Journal of Neurochemistry
|June 18, 2026
Summary
Dorsal vagal complex (DVC) astrocytes adapt to estrogen levels, influencing food intake. Inhibiting these astrocytes disrupts normal feeding patterns, revealing their role in energy homeostasis.
Area of Science:
- Neuroscience
- Endocrinology
- Astrocyte Biology
Background:
- Dorsal vagal complex (DVC) astrocytes regulate food intake and energy balance.
- Glutamatergic signaling from DVC astrocytes to dorsal motor nucleus of the vagus (DMV) motoneurons is crucial for caloric homeostasis.
- Food intake in female rats varies with the estrus cycle, decreasing during high estrogen periods.
Purpose of the Study:
- To investigate the role of DVC astrocyte adaptation in estrus cycle-dependent food intake fluctuations.
- To determine the mechanisms underlying estrogen's influence on feeding behavior via DVC astrocytes and NMDA signaling.
Main Methods:
- Immunohistochemistry to assess astrocyte changes (GFAP-IR, morphology) across the estrus cycle.
- Chemogenetics to manipulate DVC astrocyte activity.
- Electrophysiology to record DMV neuron activity.
- Pharmacological interventions targeting estrogen receptors and brainstem astrocytes.
Main Results:
- Increased GFAP-IR and astrocyte complexity correlated with high estrogen levels.
- DVC astrocyte inhibition abolished food intake oscillations; activation decreased food intake.
- Estrus-dependent feeding changes involved DMV NMDA receptor activation, modulated by estrogen and astrocytes.
Conclusions:
- DVC astrocytes play a fundamental role in estrogen-mediated regulation of food intake and energy homeostasis.
- Astrocyte and NMDA receptor signaling are key mediators of estrus cycle-dependent feeding patterns.
- These findings highlight astrocytes as critical regulators of hormonal influences on appetite.
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