Naus C C, Cimino M, Wood G R, Di Luca M, Cattabeni F
Department of Anatomy, University of Western Ontario, London, Canada.
Brain Res Dev Brain Res. 1992 Nov 20;70(1):39-46. doi: 10.1016/0165-3806(92)90101-2.
Methylazoxymethanol acetate (MAM) is a mitotic inhibitor that has been used to selectively destroy neuroblasts at specific times during gestation. The administration of MAM results in a dose-dependent microencephaly. Following MAM treatment at 15 days of gestation, we have noted an increase in the level of SS immunoreactivity in the neocortex, as determined by radioimmunoassay. Northern blot analysis for preproSS mRNA revealed an increase in MAM-treated cortex. The cellular distribution of SS has been determined using in situ hybridization and immunocytochemistry. There was a 30% increase in the density of SS-immunoreactive neurons in the cortex of the MAM-treated animals. These data suggest that SS neurons in the cortex are spared following MAM treatment at GD 15.
乙酸甲基偶氮甲醇（MAM）是一种有丝分裂抑制剂，已被用于在妊娠期的特定时间选择性地破坏神经母细胞。给予MAM会导致剂量依赖性的小头畸形。在妊娠第15天进行MAM治疗后，通过放射免疫测定法，我们注意到新皮质中促甲状腺激素释放激素（SS）免疫反应性水平有所增加。对前促甲状腺激素释放激素mRNA进行的Northern印迹分析显示，经MAM处理的皮质中该mRNA有所增加。已使用原位杂交和免疫细胞化学方法确定了SS的细胞分布。在接受MAM治疗的动物的皮质中，SS免疫反应性神经元的密度增加了30%。这些数据表明，在妊娠第15天进行MAM治疗后，皮质中的SS神经元未受影响。
