Neuroscience Graduate Group, Department of Neuroscience, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Ann N Y Acad Sci. 2013 Mar;1279:54-9. doi: 10.1111/nyas.12053.
The neuronal dendritic tree is a key determinant of how neurons receive, compute, and transmit information. During early postnatal life, synaptic activity promotes dendrite elaboration. Spinal motor neurons utilize GluA1-containing AMPA (2-amino-3-(3-hydroxy-5-methyl-isoxazol-4-yl) propanoic acid) receptors (AMPA-R) to control this process. This form of developmental dendrite growth can occur independently of N-methyl-d-aspartate receptors (NMDA-R). This review focuses on the mechanism by which the GluA1 subunit of AMPA-R transforms synaptic activity into dendrite growth, and describes the essential role of the GluA1 binding partner SAP97 (synapse-associated protein of 97 kDa molecular weight) in this process. This work defines a new mechanism of activity-dependent development, which might be harnessed to stimulate the recovery of function following insult to the central nervous system.
神经元树突是神经元接收、计算和传递信息的关键决定因素。在出生后的早期，突触活动促进树突的延伸。脊髓运动神经元利用含有 GluA1 的 AMPA（2-氨基-3-(3-羟基-5-甲基异恶唑-4-基)丙氨酸）受体（AMPA-R）来控制这个过程。这种形式的发育性树突生长可以独立于 N-甲基-D-天冬氨酸受体（NMDA-R）发生。这篇综述重点介绍了 AMPA-R 的 GluA1 亚基将突触活动转化为树突生长的机制，并描述了 GluA1 结合伴侣 SAP97（分子量为 97 kDa 的突触相关蛋白）在这个过程中的重要作用。这项工作定义了一种新的活性依赖性发育机制，这可能被用来刺激中枢神经系统损伤后的功能恢复。
