Shetty A K, Turner D A
Department of Surgery (Neurosurgery), Duke University Medical Center, Durham, North Carolina 27710, USA.
J Comp Neurol. 1995 Dec 25;363(4):581-599. doi: 10.1002/cne.903630406.
Calbindin and non-phosphorylated neurofilament proteins were assessed in hippocampus following a unilateral intracerebroventricular kainic acid injection at 4, 26, and 60 days post-lesion, using immunocytochemical expression. The density of calbindin-positive non-pyramidal neurons throughout the hippocampus showed no significant alteration at 4 days post-lesion, a significant decrease at 26 days post-lesion, and a partial recovery at 60 days post-lesion. In addition, calbindin immunoreactivity was dramatically reduced at 26 days post-lesion in the CA1 pyramidal and dentate granule cell layers and the mossy fibers, bilaterally. Although not significant statistically, most of these reductions showed signs of reversal at 60 days post-lesion except the CA1 pyramidal cell layer where the dramatic reductions persisted. Neurofilaments were also altered throughout the post-lesion period, particularly in abnormal expression of non-phosphorylated neurofilament proteins in mossy fibers. The apparent return of calbindin immunoreactivity in non-pyramidal neurons by 60 days post-lesion suggests that recovery from the lesion may involve remaining neuronal elements which either become reactivated with time or have the capability to express normal levels of calbindin with re-innervation. On the other hand, prolonged calbindin reductions in superficial CA1 pyramidal cells suggest sustained down-regulation of calbindin expression owing to persistent reductions in the activity of these neurons. The temporal correlation of the expression of non-phosphorylated neurofilaments in mossy fibers with their sprouting response following target loss suggests a potential role for non-phosphorylated neurofilaments in neuronal plasticity involving axonal sprouting. Alternatively, it may also suggest that injury-induced neurofilament modifications are either conducive or permissive for axonal sprouting.
在单侧脑室内注射 kainic 酸后第 4、26 和 60 天，利用免疫细胞化学表达法评估海马体中的钙结合蛋白和非磷酸化神经丝蛋白。损伤后第 4 天，整个海马体中钙结合蛋白阳性的非锥体神经元密度无显著变化；损伤后第 26 天显著降低；损伤后第 60 天部分恢复。此外，双侧 CA1 锥体层、齿状颗粒细胞层和苔藓纤维中，损伤后第 26 天钙结合蛋白免疫反应性显著降低。尽管统计学上不显著，但除 CA1 锥体细胞层中显著降低仍持续存在外，这些降低中的大多数在损伤后第 60 天显示出逆转迹象。在整个损伤后时期神经丝也发生了改变，特别是苔藓纤维中非磷酸化神经丝蛋白的异常表达。损伤后第 60 天非锥体神经元中钙结合蛋白免疫反应性明显恢复，这表明损伤后的恢复可能涉及剩余的神经元成分，这些成分要么随时间重新激活，要么有能力在重新支配时表达正常水平的钙结合蛋白。另一方面，浅层 CA1 锥体细胞中钙结合蛋白的持续降低表明，由于这些神经元活动的持续减少，钙结合蛋白表达持续下调。苔藓纤维中非磷酸化神经丝的表达与其在靶标丧失后的发芽反应的时间相关性表明，非磷酸化神经丝在涉及轴突发芽的神经元可塑性中具有潜在作用。或者，这也可能表明损伤诱导的神经丝修饰对轴突发芽要么是有利的，要么是允许的。
