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Corticosterone effects on postnatal cerebellar development in mice.

M Hernandez1, S Ghislin2, R Lalonde2

  • 1Laboratory of Stress, Immunity, Pathogens (EA 7300), Medical School, University of Lorraine, 54500 Vandœuvre-les-Nancy, France; CHRU Nancy, Vandœuvre-les-Nancy, France.

Neurochemistry International
|September 13, 2023
PubMed
Summary

Early life glucocorticoid exposure, like corticosterone (CORT), can impair brain development, affecting motor function and cognition. This study shows CORT disrupts cerebellar and hippocampal development in infant mice, potentially causing long-term deficits.

Keywords:
CerebellumGlucocorticoidHippocampusPlasticity factorsPostnatal development

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Area of Science:

  • Neuroscience
  • Developmental Biology
  • Endocrinology

Background:

  • Early-life glucocorticoid exposure can disrupt brain development, leading to neuromotor and cognitive deficits.
  • The developing brain, particularly structures with postnatal growth, is sensitive to hormonal influences.
  • Understanding these effects is crucial for predicting long-term functional outcomes.

Purpose of the Study:

  • To investigate the impact of daily corticosterone (CORT) injections on cerebellar and hippocampal development in infant mice.
  • To analyze gene expression of key neurotrophic factors and receptors.
  • To assess morphological and metabolic changes in brain regions critical for motor control.

Main Methods:

  • Daily administration of pharmacological doses of CORT to mouse pups from postnatal days 8-15.
  • Analysis of gene expression (mRNA levels) for HPA axis components, neurotrophic factors (BDNF), and receptors (GR, TrkB) in the hippocampus and cerebellum.
  • Histological analysis of layer thickness and cytochrome oxidase labeling to assess morphology and metabolic activity in the hippocampus and cerebellum.

Main Results:

  • CORT treatment dysregulated the HPA axis, increasing hypothalamic Crh and Nr3c1 mRNA and serum corticosterone levels.
  • Hippocampal morphology was altered, with down-regulation of Crh, Crhr1, Nr3c1, Bdnf, and Ntrk2 gene expression.
  • Cerebellar lobules showed morphological alterations and metabolic changes; the paramedian lobule was atrophic but hyperactive, while others displayed delayed synaptogenesis.

Conclusions:

  • Daily glucocorticoid administration during the second postnatal week significantly alters hippocampal and cerebellar development in mice.
  • These developmental programming changes, including altered gene expression and morphology, may lead to lasting functional deficits.
  • The findings highlight the critical vulnerability of the early-life brain to glucocorticoid exposure.