Abe K, Kitagawa H, Setoguchi Y
Department of Neurology, Okayama University School of Medicine, Japan.
Neurol Res. 1998 Dec;20(8):689-96. doi: 10.1080/01616412.1998.11740585.
A replication-defective adenoviral vector containing the E. coli lacZ gene was directly injected into normal and post-ischemic gerbil right hippocampus and lateral ventricle, and temporal profiles of the exogenous gene expression were compared. In case of ischemia, common carotid arteries (CCA) were transiently occluded for 5 min, and the adenoviral vector was administered just after the reperfusion. The animals were recovered for 8 h, 1, 3, 7 or 21 days. A small to moderate number of neural cells in the normal hippocampus expressed the gene from 1-3 days except for the cells around dentate gyrus (DG) and the needle route that began to express from 8 h of injection. Some normal hippocampal cells persisted the expression until 7 days. A moderate to large number of ventricular cells expressed the lacZ gene from 8 h to 7 days in the normal brain. On the other hand, no expression of the lacZ gene was observed in the post-ischemic hippocampus at 8 h including cells at DG and the needle route. Hippocampal CA1 neurons, that were selectively lost at 7 days of reperfusion, never expressed the gene throughout the post-ischemic course. The other hippocampal cells such as CA3 and dentate granule cells that survived ischemia expressed the gene only transiently at 1 day. A robust expression of the gene persisted in the ventricular cells from 8 h to 7 days. The majority of brain cells in the hippocampus that expressed the lacZ gene was not the pyramidal neurons, but small neurons at around the pyramidal layers of DG. Some astroglial, but no microglial, cells expressed the lacZ gene in the hippocampus. The present study shows that an expression of the lacZ gene was limited in the post-ischemic gerbil hippocampus especially at the vulnerable CA1 layer in contrast to the strong and persistent expression in the ventricular cells, and that the majority of beta-gal positive cells were not the pyramidal neurons but small neurons at around the cell layer both in the control and post-ischemic gerbil hippocampus.
将携带大肠杆菌β-半乳糖苷酶（lacZ）基因的复制缺陷型腺病毒载体直接注射到正常及缺血后的沙鼠右侧海马体和侧脑室中，并比较外源基因表达的时间变化情况。对于缺血组，暂时阻断双侧颈总动脉（CCA）5分钟，在再灌注后立即注射腺病毒载体。动物恢复8小时、1天、3天、7天或21天。在正常海马体中，除齿状回（DG）周围的细胞以及从注射后8小时开始表达的针道周围细胞外，少量至中等数量的神经细胞在1 - 3天表达该基因。一些正常海马体细胞持续表达至7天。在正常大脑中，中等数量至大量的脑室细胞从8小时至7天表达lacZ基因。另一方面，在缺血后8小时的海马体中未观察到lacZ基因表达，包括DG处的细胞和针道周围细胞。在再灌注7天时选择性丢失的海马CA1神经元在整个缺血后过程中从未表达该基因。其他在缺血中存活的海马细胞，如CA3和齿状颗粒细胞，仅在1天短暂表达该基因。脑室细胞中该基因从8小时至7天持续强劲表达。海马体中表达lacZ基因的大多数脑细胞不是锥体细胞，而是DG锥体细胞层周围的小神经元。海马体中有一些星形胶质细胞表达lacZ基因，但没有小胶质细胞表达。本研究表明，与脑室细胞中强劲且持续的表达相比，lacZ基因在缺血后的沙鼠海马体中表达受限，尤其是在易损的CA1层，并且在对照和缺血后的沙鼠海马体中，大多数β-半乳糖苷酶阳性细胞不是锥体细胞，而是细胞层周围的小神经元。
