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Open Access Research article

Prenatal cocaine exposure alters alpha2 receptor expression in adolescent rats

Rosemarie M Booze12*, David R Wallace3, Janelle M Silvers12, Barbara J Strupp4, Diane M Snow5 and Charles F Mactutus1

Author Affiliations

1 Department of Psychology, University of South Carolina Columbia, SC 29208, USA

2 Department of Pharmacology, Physiology and Neuroscience, University of South Carolina Columbia, SC 29208, USA

3 Department of Pharmacology and Physiology, Oklahoma State University, College of Osteopathic Medicine Tulsa, OK 74017-1898, USA

4 Division of Nutritional Sciences and Department of Psychology, Cornell University Ithaca, NY 14853-6301, USA

5 Department of Anatomy and Neurobiology, The University of Kentucky, Lexington, KY 40536-0298, USA

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BMC Neuroscience 2006, 7:33  doi:10.1186/1471-2202-7-33

Published: 18 April 2006



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 α2-adrenergic receptor (α2-AR) density in adolescent (35-days-old) rats, using [3H]RX821002 (5 nM).


Sex-specific alterations of α2-AR were found in the hippocampus and amygdala of the cocaine-exposed animals, as well as an upregulation of α2-AR in parietal cortex.


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.