He Kaiwen, Goel Anubhuti, Ciarkowski Claire E, Song Lihua, Lee Hey-Kyoung
Department of Biology; University of Maryland; College Park, MD USA.
Commun Integr Biol. 2011 Sep;4(5):569-72. doi: 10.4161/cib.4.5.15890. Epub 2011 Sep 1.
Regulation of synaptic AMPA receptors (AMPARs) is one of the key elements that allow the nervous system to adapt to changes in the sensory environment as well as for memory formation. One way to regulate AMPAR function is by reversible changes in the phosphorylation of its subunits. We recently reported that phosphorylation of the AMPAR subunit GluA1 (or GluR1) on serine-845 (S845) is a pre-requisite step for sensory experience-dependent homeostatic synaptic plasticity in the visual cortex. In particular, increasing GluA1-S845 phosphorylation upregulated cell surface and synaptic AMPAR levels. Here we report that this is rather specific to the visual cortex, in that increasing GluA1-S845 phosphorylation in hippocampal slices only increase cell surface expression, but not synaptic AMPAR function. Our results suggest that depending on the brain region divergent mechanisms may exist to regulate synaptic AMPAR function with phosphorylation.
突触α-氨基-3-羟基-5-甲基-4-异恶唑丙酸受体(AMPARs)的调节是使神经系统能够适应感觉环境变化以及形成记忆的关键因素之一。调节AMPAR功能的一种方式是通过其亚基磷酸化的可逆变化。我们最近报道,AMPAR亚基GluA1(或GluR1)在丝氨酸845(S845)位点的磷酸化是视觉皮层中依赖感觉经验的稳态突触可塑性的一个先决步骤。特别是,增加GluA1-S845磷酸化会上调细胞表面和突触AMPAR水平。在此我们报告,这在视觉皮层中具有相当的特异性,因为在海马切片中增加GluA1-S845磷酸化仅增加细胞表面表达,而不增加突触AMPAR功能。我们的结果表明,根据脑区的不同,可能存在不同的机制通过磷酸化来调节突触AMPAR功能。