Morrow Bret A, Hajszan Tibor, Leranth Csaba, Elsworth John D, Roth Robert H
Department of Psychiatry, Neuropsychopharmacology Research Unit, Yale University School of Medicine, New Haven, CT 06511, USA.
Synapse. 2007 Oct;61(10):862-5. doi: 10.1002/syn.20430.
Prenatal exposure to cocaine has been associated with cognitive deficits in children and in animal models. An excess activation of pyramidal neurons in the prefrontal cortex has been proposed as a potential cause for these deficits based on previous studies. The goal of this study was to determine if prenatal exposure to cocaine was associated with an increase in the number of excitatory synapses on dendritic spines in layer II/III of the prelimbic cortex. Frontal cortex of young adult male and female rats, exposed to either saline or cocaine (3 mg/kg i.e., twice a day, embryonic day 10-20), were examined using electron microscopy and the number of asymmetric spines synapses were estimated using the physical disector method. Both male and female rats prenatally exposed to cocaine had about twice as many synapses on dendritic spines as the prenatal saline controls. The increase in number of excitatory synaptic inputs associated with prenatal cocaine exposure could contribute to the increased neuronal activation and cognitive deficits noted.
产前接触可卡因已被证明与儿童及动物模型中的认知缺陷有关。基于先前的研究，前额叶皮质锥体细胞的过度激活被认为是导致这些缺陷的潜在原因。本研究的目的是确定产前接触可卡因是否与前边缘皮质II/III层树突棘上兴奋性突触数量的增加有关。使用电子显微镜检查了产前暴露于生理盐水或可卡因（3mg/kg，即每天两次，胚胎期第10至20天）的年轻成年雄性和雌性大鼠的额叶皮质，并使用物理分割法估计不对称棘突触的数量。产前接触可卡因的雄性和雌性大鼠在树突棘上的突触数量大约是产前生理盐水对照组的两倍。与产前可卡因暴露相关的兴奋性突触输入数量的增加可能导致所观察到的神经元激活增加和认知缺陷。
