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Prenatal glucocorticoid programming of brain corticosteroid receptors and corticotrophin-releasing hormone: possible

L A Welberg1, J R Seckl, M C Holmes

  • 1Molecular Endocrinology Laboratory, Molecular Medicine Centre, University of Edinburgh, Western General Hospital, EH4 2XU, Scotland, Edinburgh, UK.

Neuroscience
|April 20, 2001
PubMed

Insights

Prenatal exposure to dexamethasone (a glucocorticoid) in rats reduced birth weight and adult exploratory behavior. Late-gestation exposure specifically impaired coping and learning, potentially linking early growth restriction to adult affective dysfunction.

Area of Science:

  • Neuroendocrinology
  • Developmental Neuroscience
  • Behavioral Pharmacology

Background:

  • Low birth weight is associated with adult disorders like hypertension, type 2 diabetes, and affective dysfunction.
  • Glucocorticoids are implicated in mediating the link between early growth and adult health outcomes.
  • Prenatal exposure to glucocorticoids may program long-term behavioral and molecular changes.

Purpose of the Study:

  • To investigate the behavioral and molecular effects of two distinct prenatal dexamethasone exposure paradigms in rats.
  • To determine if the timing of prenatal glucocorticoid exposure influences adult behavioral outcomes and stress axis regulation.
  • To explore the potential mechanisms underlying the association between prenatal glucocorticoid exposure and adult affective dysfunction.

Main Methods:

  • Rats received dexamethasone throughout pregnancy (DEX1-3) or in the last third (DEX3), with a control group receiving vehicle.
  • Behavioral assessments included open field, elevated plus-maze, and forced-swim tests.
  • Molecular analyses measured mRNA levels of corticotrophin-releasing hormone and corticosteroid receptors in the amygdala and hippocampus.

Main Results:

  • Both dexamethasone treatments reduced birth weight; only DEX1-3 reduced adult body weight.
  • Prenatal dexamethasone reduced exploratory behavior in both paradigms.
  • DEX3 specifically impaired coping and learning, associated with altered hippocampal and amygdalar gene expression.
  • Increased central amygdala corticotrophin-releasing hormone mRNA was observed in both treatment groups.

Conclusions:

  • Prenatal glucocorticoid exposure can program behavioral inhibition, potentially mediated by amygdalar corticotrophin-releasing hormone.
  • Late-gestation exposure (DEX3) may lead to impaired coping and learning due to altered hippocampal corticosteroid receptor sensitivity.
  • These findings suggest a mechanism linking reduced early growth and prenatal glucocorticoid exposure to adult affective dysfunction.

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