Molecular basis of neural plasticity in the hippocampus.

为了阐明神经元可塑性的分子机制，我们研究了诱导点燃或长时程增强后大鼠海马基因表达和蛋白质磷酸化的具体变化。对从点燃海马和对照海马制备的消减cDNA文库进行分子克隆。细胞色素氧化酶亚基 2 和 3 的基因表达因点燃而升高。在点燃后的海马体和大脑皮层上研究了钙/钙调蛋白依赖性激酶 II 的蛋白质磷酸化。尽管酶活性没有显着改变，但点燃的海马体和皮质中突触蛋白 I 的磷酸化升高。在体外研究了突触体部分的谷氨酸释放。高钾刺激导致点燃的皮层释放更多。

In order to elucidate the molecular mechanism of neuronal plasticity, we investigated specific changes in gene expression and protein phosphorylation of the rat hippocampus after kindling or long-term potentiation was induced. Molecular cloning was performed on the subtracted cDNA library prepared from kindled and control hippocampi. Expression of genes for cytochrome oxidase subunits 2 and 3 was elevated by kindling. Protein phosphorylation by calcium/calmodulin-dependent kinase II was investigated on the hippocampus and cerebral cortex after kindling. Although enzyme activity was not altered significantly, phosphorylation of synapsin I was elevated in kindled hippocampus and cortex. Glutamate release from synaptosome fraction was investigated in vitro. High potassium stimulation induced the more release from kindled cortex.