Prenatal glucocorticoid exposure affects learning and vulnerability of cholinergic neurons

Neurobiol Aging. 2007 Jan;28(1):112-21. doi: 10.1016/j.neurobiolaging.2005.11.015. Epub 2006 Jan 6.


Prenatal treatment with synthetic glucocorticoids is commonly used as a treatment for women at risk of preterm delivery. However, little is known about the life-long consequences of these treatments on the fetus. In the present study, we evaluated cognitive function as well as susceptibility of cholinergic neurons to (192)IgG-saporin immunolesion in adult rats after prenatal glucocorticoid treatment. Morris water maze results revealed a significant difference in learning and memory function in adult rats that were prenatally exposed to dexamethasone, and further cognitive deficits after (192)IgG-saporin exposure. Choline acetyl transferase activity was decreased in the cortex of dexamethasone-treated rats compared with controls. In addition, rats prenatally exposed to either dexa, or betamethasone revealed a dramatic decrease in choline acetyl transferase activity compared to control rats after (192)IgG-saporin lesion. We report behavioral and biochemical evidence for altered cognitive function and increased susceptibility of cholinergic neurons to (192)IgG-saporin in adult rats after prenatal glucocorticoid treatment. Taken together, these results suggest that prenatal treatment with dexamethasone could affect cognitive functions and render cholinergic neurons more vulnerable to challenges later in life.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cerebral Cortex / drug effects
  • Cerebral Cortex / metabolism
  • Cognition Disorders / chemically induced
  • Cognition Disorders / physiopathology
  • Dexamethasone / adverse effects*
  • Disease Susceptibility / chemically induced
  • Disease Susceptibility / physiopathology
  • Female
  • Male
  • Maternal-Fetal Exchange
  • Maze Learning / drug effects*
  • Maze Learning / physiology*
  • Neurons / metabolism*
  • Pregnancy
  • Prenatal Exposure Delayed Effects / chemically induced*
  • Prenatal Exposure Delayed Effects / physiopathology*
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Nicotinic / metabolism*


  • Receptors, Nicotinic
  • Dexamethasone