Johnston H M, Morris B J
Department of Pharmacology, University of Glasgow, Scotland.
J Neurochem. 1994 Jul;63(1):379-82. doi: 10.1046/j.1471-4159.1994.63010379.x.
Microtubule-associated protein 2 (MAP2), a component of the neuronal cytoskeleton, has attracted attention as a possible cellular substrate linking hippocampal N-methyl-D-aspartate (NMDA) receptor stimulation to alterations in cellular morphology. We show here that microinjection of NMDA, 8-bromo-cyclic GMP, or sin-1 molsidomine (which spontaneously releases nitric oxide), onto the molecular layer of the hippocampal dentate gyrus, increased the levels of MAP2 mRNA in the affected granule cells. No changes were observed in the levels of mRNAs encoding several other cytoskeletal components. This shows that hippocampal NMDA receptor stimulation can potentially initiate a long-term alteration in dendritic structure by affecting MAP2 gene expression and provides the first evidence that nitric oxide release in vivo, acting through cyclic GMP-dependent protein kinase, can cause long-term changes in neuronal function by modulating gene expression.
微管相关蛋白2（MAP2）是神经元细胞骨架的一个组成部分，作为一种可能将海马N-甲基-D-天冬氨酸（NMDA）受体刺激与细胞形态改变联系起来的细胞底物而受到关注。我们在此表明，将NMDA、8-溴环鸟苷或辛-1（可自发释放一氧化氮）微量注射到海马齿状回的分子层上，可增加受影响颗粒细胞中MAP2 mRNA的水平。编码其他几种细胞骨架成分的mRNA水平未观察到变化。这表明海马NMDA受体刺激可能通过影响MAP2基因表达而引发树突结构的长期改变，并首次证明体内释放的一氧化氮通过环鸟苷依赖性蛋白激酶起作用，可通过调节基因表达导致神经元功能的长期变化。
