Fujimoto Takahiro, Tanaka Hidekazu, Kumamaru Emi, Okamura Ko, Miki Naomasa
Department of Pharmacology, Osaka University Medical School, Suita, Osaka, Japan.
J Neurosci Res. 2004 Apr 1;76(1):51-63. doi: 10.1002/jnr.20056.
Arc, activity-regulated cytoskeleton-associated gene, is an immediate early gene, and its expression is regulated by a variety of stimuli, such as electric stimulation and methamphetamine. The function of Arc, however, is unknown. To explore this function, we carried out expression experiments by transfecting green fluorescent protein (GFP)-Arc constructs or by using a protein transduction system in hippocampal cultured neurons. We found that the overexpression of Arc as well as Arc induction by seizure in vivo decreased microtubule-associated protein 2 (MAP2) staining in the dendrites by immunocytochemistry, although MAP2 content was not changed on Western blot. Furthermore, Arc interacted with newly polymerized microtubules and MAP2, leading to blocking of the epitope of MAP2. The data suggest that Arc increased by synaptic activities would trigger dendritic remodeling by interacting with cytoskeletal proteins.
Arc，即活动调节细胞骨架相关基因，是一种立早基因，其表达受多种刺激调控，如电刺激和甲基苯丙胺。然而，Arc的功能尚不清楚。为探究该功能，我们在海马体培养神经元中通过转染绿色荧光蛋白（GFP）-Arc构建体或使用蛋白质转导系统进行了表达实验。我们发现，通过免疫细胞化学方法，Arc的过表达以及体内癫痫发作诱导的Arc均使树突中微管相关蛋白2（MAP2）染色减少，尽管在蛋白质印迹法中MAP2含量未发生变化。此外，Arc与新聚合的微管和MAP2相互作用，导致MAP2表位被阻断。这些数据表明，由突触活动增加的Arc会通过与细胞骨架蛋白相互作用触发树突重塑。
