Lidow M S, Bozian D, Song Z M
Department of Oral and Craniofacial Biological Sciences and Program of Neuroscience, University of Maryland, Baltimore, 5-A-12, HHH, 666 W. Baltimore Street, Baltimore, MD 21201, USA.
Brain Res Dev Brain Res. 2001 May 31;128(1):45-52. doi: 10.1016/s0165-3806(01)00139-0.
Previously, we demonstrated that chronic exposure of fetal monkeys to cocaine could result in development of the neocortex with significant cytoarchitectonic abnormalities [Synapse, 21 (1995) 435-444]. In the present study, we examined the developmental time-frame within which neocortical cytoarchitecture is susceptible to modifications by prenatal cocaine exposure. For this purpose, we assessed the integrity of cortical lamination and the position, density, and total number of occipital cortical neurons in 2-month-old monkeys which were prenatally exposed to chronic cocaine treatment either prior to the period of neocortical neuronogenesis, during the period of neocortical neuronogenesis, or after the period of neocortical neuronogenesis. We found that cocaine can interfere with the neocortical laminar organization and induce a reduction in the density and number of neocortical neurons only if it is administered at the time of neocortical neuronogenesis. During this window of vulnerability, an abnormal neocortex is generated as long as cocaine exposure is maintained, with corticogenesis becoming normal as soon as the administration of this drug is discontinued.
此前，我们证明，将胎猴长期暴露于可卡因环境中，可导致新皮质发育出现显著的细胞结构异常[《突触》，21(1995)435 - 444]。在本研究中，我们探究了新皮质细胞结构易受产前可卡因暴露影响而发生改变的发育时间范围。为此，我们评估了2月龄猴子的皮质分层完整性以及枕叶皮质神经元的位置、密度和总数，这些猴子在新皮质神经发生期之前、新皮质神经发生期或新皮质神经发生期之后，均在产前接受了长期可卡因治疗。我们发现，只有在新皮质神经发生期给予可卡因，它才会干扰新皮质的分层组织，并导致新皮质神经元密度和数量减少。在这个易损期内，只要持续暴露于可卡因，就会产生异常的新皮质，而一旦停止使用该药，皮质发生就会恢复正常。
