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Does prenatal stress impair coping and regulation of hypothalamic-pituitary-adrenal axis?

M Weinstock1

  • 1Department of Pharmacology, School of Pharmacy, Hebrew University, Hadassah Medical Centre, Ein Kerem, Jerusalem, Israel.

Neuroscience and Biobehavioral Reviews
|January 1, 1997
PubMed

Insights

Prenatal stress in humans and animals leads to lasting behavioral and HPA axis issues. Maternal stress hormones acting on the fetus may explain these changes, increasing depression risk.

Area of Science:

  • Neuroscience
  • Developmental Psychology
  • Endocrinology

Background:

  • Prenatal stress (PS) in humans and animals is linked to attention deficits, anxiety, and social behavior issues.
  • Adult PS rodents and monkeys exhibit impaired coping and hypothalamic-pituitary-adrenal (HPA) axis dysregulation, including reduced feedback inhibition and elevated glucocorticoids.
  • PS rats show altered neurochemical profiles, with higher amygdala corticotropin-releasing hormone (CRH) and reduced hippocampal glucocorticoid receptors.

Purpose of the Study:

  • To investigate the mechanisms underlying long-lasting neurodevelopmental changes induced by maternal stress.
  • To explore the role of maternal hormones during gestation in fetal neuroaxis development.
  • To examine the potential link between gestational stress and an increased propensity for depression.

Main Methods:

  • This study reviews existing research on prenatal stress effects in human infants and animal models.
  • It analyzes neuroendocrine and behavioral outcomes associated with prenatal stress exposure.
  • Comparative analysis of HPA axis function, neurochemical changes, and coping behaviors in PS subjects.

Main Results:

  • Prenatal stress is associated with significant attentional deficits, hyperanxiety, and altered social behaviors.
  • HPA axis dysregulation, characterized by diminished feedback inhibition and prolonged glucocorticoid elevation, is a key finding in adult PS subjects.
  • Neurobiological correlates include increased amygdala CRH, reduced hippocampal glucocorticoid receptors, and decreased inhibitory neurotransmitter activity.

Conclusions:

  • Maternal stress hormones acting on the developing fetus are suggested as the mechanism for long-lasting neurodevelopmental alterations.
  • Gestational stress may prime the developing brain, increasing vulnerability to stress-related disorders.
  • The observed similarities between PS animal models and human depression suggest prenatal stress as a potential risk factor for mood disorders.

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