Lumme A, Soinila S, Sadeniemi M, Halonen T, Vanhatalo S
Department of Anatomy, Institute of Biomedicine, P.O. Box 9, 00014 University of Helsinki, Helsinki, Finland.
Brain Res. 2000 Jul 21;871(2):303-10. doi: 10.1016/s0006-8993(00)02487-2.
Nitric oxide has recently been implicated in mediation of neuronal excitotoxicity and damage. This study aimed at elucidating the changes in the expression of neuronal isoform of nitric oxide synthase (nNOS) in the hippocampus after status epilepticus induced by perforant pathway stimulation. nNOS-immunoreactivity (nNOS-ir) and neuronal damage, assessed by silver staining, were evaluated separately in different hippocampal subfields 2 weeks after induction of status epilepticus. Perforant pathway stimulation resulted in an increase in the number of nNOS-immunoreactive neurons in the stratum radiatum of the CA1 and CA3 subfields of the hippocampus proper, and the hilus of the dentate gyrus. The morphology and distribution of the nNOS-ir neurons resembled that of interneurons. No correlation of the number of nNOS-ir neurons to the neuronal damage score was observed. Our results suggest that status epilepticus provokes a de novo expression of nNOS protein, and the nNOS expressing neurons may be selectively resistant to epileptic brain injury.
一氧化氮最近被认为参与了神经元兴奋性毒性和损伤的介导过程。本研究旨在阐明在穿通通路刺激诱导癫痫持续状态后，海马中神经元型一氧化氮合酶（nNOS）表达的变化。在癫痫持续状态诱导2周后，分别在不同的海马亚区评估nNOS免疫反应性（nNOS-ir）和通过银染评估的神经元损伤。穿通通路刺激导致海马体CA1和CA3亚区的辐射层以及齿状回的门区中nNOS免疫反应性神经元数量增加。nNOS-ir神经元的形态和分布与中间神经元相似。未观察到nNOS-ir神经元数量与神经元损伤评分之间的相关性。我们的结果表明，癫痫持续状态引发了nNOS蛋白的从头表达，并且表达nNOS的神经元可能对癫痫性脑损伤具有选择性抗性。
