Prenatal cocaine exposure alters alpha2 receptor expression in adolescent rats

BMC Neurosci. 2006 Apr 18;7:33. doi: 10.1186/1471-2202-7-33.


Background: Prenatal cocaine exposure produces attentional deficits which to persist through early childhood. Given the role of norepinephrine (NE) in attentional processes, we examined the forebrain NE systems from prenatal cocaine exposed rats. Cocaine was administered during pregnancy via the clinically relevant intravenous route of administration. Specifically, we measured alpha2-adrenergic receptor (alpha2-AR) density in adolescent (35-days-old) rats, using [3H]RX821002 (5 nM).

Results: Sex-specific alterations of alpha2-AR were found in the hippocampus and amygdala of the cocaine-exposed animals, as well as an upregulation of alpha2-AR in parietal cortex.

Conclusion: These data suggest that prenatal cocaine exposure results in a persistent alteration in forebrain NE systems as indicated by alterations in receptor density. These neurochemical changes may underlie behavioral abnormalities observed in offspring attentional processes following prenatal exposure to cocaine.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Adrenergic alpha-Antagonists / metabolism
  • Adrenergic alpha-Antagonists / pharmacology
  • Age Factors
  • Animals
  • Autoradiography
  • Body Weight
  • Cocaine / pharmacology*
  • Dopamine Uptake Inhibitors / pharmacology*
  • Female
  • Idazoxan / analogs & derivatives
  • Idazoxan / metabolism
  • Idazoxan / pharmacology
  • Male
  • Pregnancy
  • Prenatal Exposure Delayed Effects*
  • Prosencephalon / drug effects
  • Prosencephalon / metabolism*
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Adrenergic, alpha-2 / metabolism*
  • Sexual Maturation
  • Tritium


  • Adrenergic alpha-Antagonists
  • Dopamine Uptake Inhibitors
  • Receptors, Adrenergic, alpha-2
  • Tritium
  • 2-methoxyidazoxan
  • Cocaine
  • Idazoxan