Wang Yanling, Barbaro Michael F, Baraban Scott C
Epilepsy Research Laboratory in the Department of Neurological Surgery and PIBS Graduate Program in Neuroscience, University of California, Box 0520, 513 Parnassus Ave., San Francisco, CA 94143, USA.
Neurosci Lett. 2006 Jun 19;401(1-2):35-9. doi: 10.1016/j.neulet.2006.03.011. Epub 2006 May 3.
Delivery of alpha-amino-3-hydroxy-5-methylisoxazole-4-proprionate receptors (AMPARs) to the synapse is a critical factor controlling synaptic strength. It is now established that blockade of synaptic activity increases the surface expression of AMPARs. Factors modulating the delivery, insertion and expression of AMPARs are not completely known. Using immunohistochemical techniques, we first confirmed rapamycin-mediated inhibition of the mammalian target of rapamycin (mTOR) pathway in cortical neuronal culture. We then demonstrated that acute AMPAR activity blockade increased the synaptic expression of GluR2/3 subunits and rapamycin significantly reduced this expression. Our results suggest a role for the mTOR pathway in surface expression of AMPA receptors on cortical neurons.
α-氨基-3-羟基-5-甲基异恶唑-4-丙酸受体(AMPARs)向突触的传递是控制突触强度的关键因素。现已证实,突触活动的阻断会增加AMPARs的表面表达。调节AMPARs传递、插入和表达的因素尚不完全清楚。我们首先使用免疫组织化学技术在皮质神经元培养物中证实了雷帕霉素介导的对哺乳动物雷帕霉素靶蛋白(mTOR)途径的抑制作用。然后我们证明,急性AMPAR活性阻断增加了GluR2/3亚基的突触表达,而雷帕霉素显著降低了这种表达。我们的结果表明mTOR途径在皮质神经元上AMPA受体的表面表达中发挥作用。