# Prenatal photoperiod action in hypothalamic development

> **NIH NIH R21** · UNIVERSITY OF MICHIGAN AT ANN ARBOR · 2022 · $195,000

## Abstract

ABSTRACT
Seasonal or photoperiodic changes in humans affect hormonal patterns, brain function, and are an underlying
cause of several psychological disorders. Season of birth has a clear impact on birth weight and ulterior
susceptibility to disease (e.g., childhood diabetes, psychiatry disorders and Alzheimer). Exposure to “winter-
like” short photoperiod during pregnancy delays the developmental trajectory in offspring of seasonal species.
This effect, mediated by transplacental melatonin action, leads to postnatal changes in hypothalamic thyroid
hormone (TH) regulation. In vertebrates, postembryonic brain development is critically dependent on TH,
essential in the control of neurogenesis and neuronal differentiation. Whether photoperiod affects brain
development in non-seasonal species remains unknown. We hypothesize that photoperiod impacts perinatal
hypothalamic development via local changes in TH regulation. In rodents, the embryonic program of
hypothalamic neurogenesis is completed by the end of gestation, while gliogenesis continues into the early
postnatal period. Increased TH promotes the end of proliferation of neural progenitors and favors their
neuronal instead of glial differentiation. Short photoperiod – associated with lower hypothalamic TH content –
promotes cell proliferation and increase in neural progenitor markers in adults of seasonal species. In this
application, we will initially use single cell RNA sequencing to determine the impact of distinct photoperiod
exposure during gestation on cell type specification and differentiation of the mediobasal hypothalamus during
early postnatal development (Aim 1). In Aim 2, we will use histological techniques and markers of cell
differentiation to determine if exposure to short photoperiod during gestation affects cell proliferation, newborn
cell fate program and changes in postnatal hypothalamic development. To accomplish our goals, we will use a
highly validated wild-derived mouse model in which photoperiod affects neonatal hypothalamic TH regulation.
This mouse model (Mus musculus molossinus) shows photoperiodic changes in melatonin and adult
physiology (i.e., changes in body weight and gonads size). Our overall objectives in this exploratory and
development research application are to assess the accuracy of our model, to validate the experimental mouse
and to gain knowledge on single cell hypothalamic transcriptome program during early postnatal development.
If demonstrated, our model will break new ground on the impact of photoperiod on the developing brain, and
will open new opportunities for the scientific and clinical understanding of the mechanisms by which the
seasonal environment alters hypothalamic development, neuroendocrine function, and human’s health

## Key facts

- **NIH application ID:** 10509412
- **Project number:** 1R21HD109485-01
- **Recipient organization:** UNIVERSITY OF MICHIGAN AT ANN ARBOR
- **Principal Investigator:** Carol Fuzeti Elias
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $195,000
- **Award type:** 1
- **Project period:** 2022-09-08 → 2024-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10509412

## Citation

> US National Institutes of Health, RePORTER application 10509412, Prenatal photoperiod action in hypothalamic development (1R21HD109485-01). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/10509412. Licensed CC0.

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