Qiang Mei, Wang Ming Wei, Elberger Andrea J
Department of Anatomy and Neurobiology, The University of Tennessee Health Science Center, 855 Monroe Avenue, Memphis 38163, USA.
Neurotoxicol Teratol. 2002 Nov-Dec;24(6):719-32. doi: 10.1016/s0892-0362(02)00267-2.
Prenatal alcohol exposure produces many developmental defects of the central nervous system (CNS), such as in the corpus callosum (CC). This study was designed to observe the effect of prenatal alcohol exposure during the second trimester equivalent on the development of dendritic arbors of CC projection neurons (CCpn) in rat visual cortex. In addition, the effect of second trimester equivalent prenatal alcohol exposure on brain weight was determined. Pregnant dams received 1.2-6.0 g/kg ethanol (EtOH) during gestational day (G) 11-20. Controls consisted of normal and nutritionally matched pairfed (PF) dams. Pups were sacrificed on the day of birth, G26, G29 and G33. DiI crystals were placed in the midsagittal CC bundle to retrogradely label CCpn. Images of visual cortex were obtained from tissue slices using a confocal laser scanning microscope. The number and length of apical and basilar dendrite branches were determined. The results show that prenatal alcohol exposure restricted to the second trimester equivalent alters the development of the CCpn dendritic arbor and the brain weight in a blood alcohol concentration (BAC)-dependent manner. The alteration in the EtOH CCpn is manifested as an increase in the number and length of CCpn apical and basilar dendrite branches, while brain weight is reduced compared with Controls.
产前酒精暴露会导致中枢神经系统（CNS）出现许多发育缺陷，比如胼胝体（CC）。本研究旨在观察孕中期等量酒精暴露对大鼠视觉皮层中胼胝体投射神经元（CCpn）树突分支发育的影响。此外，还确定了孕中期等量产前酒精暴露对脑重量的影响。怀孕母鼠在妊娠第11 - 20天接受1.2 - 6.0 g/kg乙醇（EtOH）。对照组包括正常且营养匹配的配对喂养（PF）母鼠。幼崽在出生当天、第26天、第29天和第33天被处死。将碘化丙啶晶体置于矢状中胼胝体束中以逆行标记CCpn。使用共聚焦激光扫描显微镜从组织切片获取视觉皮层图像。测定顶树突和基底树突分支的数量和长度。结果表明，仅限于孕中期等量的产前酒精暴露以血酒精浓度（BAC）依赖的方式改变了CCpn树突分支的发育和脑重量。EtOH处理的CCpn的改变表现为CCpn顶树突和基底树突分支的数量和长度增加，而与对照组相比脑重量减轻。
