Skip to main content
NUTRITION 2026 Main banner

(PTFS10-05-26) Vitamin D Deficiency Alters Gene Expression in the Mouse Central Amygdala

Sunday, July 26, 2026
2:46 PM - 2:50 PM ET
Location: Prince George's Hall B-E (The Hub) - Poster Theater 2 / Poster Board Number: PT2-5

    Presenting Author(s)

  • Yuhan Wang, PhD (she/her/hers)

    Assistant Professor
    Cornell University
    Ithaca, New York, United States

    Disclosure(s): No relevant financial relationship(s) with ineligible companies to disclose.

    • Co-Author(s)

  • ZW

    Ziyang Wang, M.S.

    Cornell University
    Ithaca, New York, United States

    • Co-Author(s)

  • RY

    Risa Yamazaki

    Cornell University, United States

Disclosure(s):
Yuhan Wang, PhD: No relevant financial relationship(s) with ineligible companies to disclose.
Objectives: Vitamin D, a secosteroid hormone and essential dietary nutrient, has been implicated in several neuropsychiatric and neurological disorders beyond its classical role in bone health. Yet, the neural mechanisms underlying these associations remain poorly understood. Previous studies, including our own work, identified a population of VitD receptor (VDR)-expressing neurons in the mouse central amygdala (CeA), a brain region critical for emotional processing and fear-related behavior. We hypothesized that VitD deficiency alters CeA neuronal function through VDR signaling and aimed to characterize the transcriptional changes induced by VitD deficiency in this region.

Methods: To examine the effects of VitD deficiency, wild-type C57BL/6J mice were placed on a VitD-deficient diet. CeA tissue was then collected from VitD deficient and control mice for RNA sequencing. Gene set enrichment analysis (GSEA) was performed using the fgsea package and enrichment was evaluated based on normalized enrichment score (NES) and p-value. Fluorescence in situ hybridization (FISH) was then used to validate gene expression changes specifically in VDR-expressing neurons in the CeA.

Results: GSEA revealed broad downregulation of VDR neuron-specific marker genes in VitD-deficient mice. Pathway analysis indicated that affected genes are enriched for processes related to ion transport, calcium homeostasis, and synaptic components, suggesting potential disruption of neuronal signaling and synaptic function within the CeA. Spatial in situanalysis further showed a reduction of Vdr expression in VitD deficient mice, suggesting that transcriptional changes observed may be driven by reduced VDR signaling.

Conclusions: These findings demonstrate that VitD deficiency induces transcriptional changes in the CeA, particularly in pathways governing ion transport, calcium signaling, and synaptic function. Given CeA's role in emotional and stress-related behavior, these changes may provide a mechanistic link between VitD deficiency and the associated neuropsychiatric symptoms. Future studies examining the behavioral consequences of CeA neuron dysregulation will be important for understanding how nutritional VitD status shapes brain function and mental health.

Funding Sources: Intramural funds