Booze Rosemarie M, Wallace David R, Silvers Janelle M, Strupp Barbara J, Snow Diane M, Mactutus Charles F
Department of Psychology, University of South Carolina Columbia, SC 29208, USA.
BMC Neurosci. 2006 Apr 18;7:33. doi: 10.1186/1471-2202-7-33.
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).
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.
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.
产前接触可卡因会导致注意力缺陷，这种缺陷会持续到幼儿期。鉴于去甲肾上腺素（NE）在注意力过程中的作用，我们研究了产前接触可卡因的大鼠的前脑NE系统。在孕期通过临床相关的静脉给药途径给予可卡因。具体而言，我们使用[3H]RX821002（5 nM）测量了青春期（35日龄）大鼠的α2-肾上腺素能受体（α2-AR）密度。
在接触可卡因的动物的海马体和杏仁核中发现了α2-AR的性别特异性改变，以及顶叶皮质中α2-AR的上调。
这些数据表明，产前接触可卡因会导致前脑NE系统的持续改变，如受体密度的改变所示。这些神经化学变化可能是产前接触可卡因后在后代注意力过程中观察到的行为异常的基础。
