Garavan H, Morgan R E, Mactutus C F, Levitsky D A, Booze R M, Strupp B J
Division of Nutritional Sciences, Cornell University, Ithaca, New York 14853-6301, USA.
Behav Neurosci. 2000 Aug;114(4):725-38.
This study assessed the effects of prenatal cocaine exposure on cognitive functioning, using an intravenous (IV) rodent model that closely mimics the pharmacokinetics seen in humans after smoking or IV injection and that avoids maternal stress and undernutrition. Cocaine-exposed males were significantly impaired on a 3-choice, but not 2-choice, olfactory serial reversal learning task. Both male and female cocaine-exposed rats were significantly impaired on extradimensional shift tasks that required shifting from olfactory to spatial cues; however, they showed no impairment when required to shift from spatial to olfactory cues. In-depth analyses of discrete learning phases implicated deficient selective attention as the basis of impairment in both tasks. These data provide clear evidence that prenatal cocaine exposure produces long-lasting cognitive dysfunction, but they also underscore the specificity of the impairment.
本研究使用一种静脉注射（IV）啮齿动物模型评估产前可卡因暴露对认知功能的影响，该模型紧密模拟人类吸烟或静脉注射后所见的药代动力学，且避免了母体应激和营养不良。在一项三选一而非二选一的嗅觉连续反转学习任务中，暴露于可卡因的雄性大鼠表现出显著受损。暴露于可卡因的雄性和雌性大鼠在需要从嗅觉线索转换为空间线索的维度外转换任务中均表现出显著受损；然而，当要求它们从空间线索转换为嗅觉线索时，它们并未表现出受损。对离散学习阶段的深入分析表明，选择性注意力缺陷是两项任务受损的基础。这些数据提供了明确的证据，表明产前可卡因暴露会产生持久的认知功能障碍，但它们也强调了这种损伤的特异性。
