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 α<sub>2</sub>-adrenergic receptor (α<sub>2</sub>-AR) density in adolescent (35-days-old) rats, using [<sup>3</sup>H]RX821002 (5 nM).
Sex-specific alterations of α<sub>2</sub>-AR were found in the hippocampus and amygdala of the cocaine-exposed animals, as well as an upregulation of α<sub>2</sub>-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.
BMC Neuroscience. 01/2006;