Nakamura M, Araki M, Oguro K, Masuzawa T
Department of Surgical Neurology, Jichi Medical School, Tochigi, Japan.
Exp Brain Res. 1992;89(1):31-9. doi: 10.1007/BF00228998.
The distribution of neurofilament (NF) proteins was studied immunohistochemically in the gerbil hippocampus with antibodies against NF68 (68 Kd molecular weight) and NF200 proteins, and changes in the distribution of NF proteins after transient ischemia were observed in order to investigate the temporal correlation between NF and delayed neuronal death. In the normal hippocampus, NF68-like immunoreactivity (NF68-LI) was densely distributed in nerve processes in CA2, CA3 and the hilus of the dentate gyrus but was less intense in CA1. In contrast, processes with NF200-LI appeared to be evenly distributed in CA1, CA2, CA3 and the dentate gyrus. Mongolian gerbils were subjected to transient ischemia for 5 min by bilateral carotid occlusion and subjected to immunohistochemistry 1, 2, 3 and 4 days after ischemia. Following transient ischemia, prior to neuronal cell death, the intensity of both NF68-LI and NF200-LI decreased in the whole hippocampal formation. This decrease was more obvious in the case of NF68-LI than NF200-LI. Four days after ischemia, when neuronal death of CA1 pyramidal cells had occurred, processes in CA1, particularly 68 Kd components, showed marked decreases in number and staining intensity, although processes in most layers of CA2, CA3 and the dentate gyrus appeared to be stained similarly to normal brain. Since NF68 protein is considered to be the major component of NF proteins and NF200 is an associated accessory protein, the current observations suggest that the poor distribution of NF68 in CA1 and the early loss of NF proteins may be closely related to selective vulnerability of CA1 pyramidal cells and delayed neuronal death.
采用抗神经丝蛋白68（NF68，分子量68千道尔顿）和NF200蛋白的抗体，通过免疫组织化学方法研究了沙鼠海马中神经丝（NF）蛋白的分布，并观察了短暂性脑缺血后NF蛋白分布的变化，以探讨NF与迟发性神经元死亡之间的时间相关性。在正常海马中，NF68样免疫反应性（NF68-LI）密集分布于CA2、CA3和齿状回门区的神经突起中，但在CA1区强度较低。相比之下，具有NF200-LI的神经突起似乎在CA1、CA2、CA3和齿状回中均匀分布。通过双侧颈动脉闭塞使蒙古沙鼠经历5分钟的短暂性脑缺血，并在缺血后1、2、3和4天进行免疫组织化学检测。短暂性脑缺血后，在神经元细胞死亡之前，整个海马结构中NF68-LI和NF200-LI的强度均降低。这种降低在NF68-LI的情况下比NF200-LI更明显。缺血4天后，当CA1锥体细胞发生神经元死亡时，CA1区的神经突起，特别是68千道尔顿的成分，在数量和染色强度上显著降低，尽管CA2、CA3和齿状回大多数层的神经突起染色似乎与正常脑相似。由于NF68蛋白被认为是NF蛋白的主要成分，而NF200是相关的辅助蛋白，目前的观察结果表明，CA1区NF68分布不佳和NF蛋白的早期丢失可能与CA1锥体细胞的选择性易损性和迟发性神经元死亡密切相关。
