Itoh Kouichi, Shimono Ken, Lemmon Vance
Laboratory of Molecular Pharmacology, Department of Pharmaceutical Technology, Faculty of Pharmaceutical Sciences at Kagawa Campus, Tokushima Bunri University, Kagawa 769-2193, Japan.
Mol Cell Neurosci. 2005 Jun;29(2):245-9. doi: 10.1016/j.mcn.2005.02.014.
The neural cell adhesion molecule L1 may participate in initiating and maintaining synaptic changes during learning in the hippocampus. One prominent form of synaptic change in the hippocampus is long-term potentiation (LTP) that occurs following specific patterns of synaptic activity. We present evidence that Y1176 of the YRSL motif within L1 cytoplasmic domain is dephosphorylated in LTP-induced hippocampus. The dephosphorylated L1 is associated with AP-2 and AP180 that are required for clathrin-mediated internalization of L1. These data suggest that clathrin-mediated recycling of L1 at presynaptic sites is enhanced by certain kinds of neural activity, and that maintenance of LTP-induced synaptic changes is regulated by L1 recycling.
神经细胞黏附分子L1可能参与海马体学习过程中突触变化的启动和维持。海马体中突触变化的一种显著形式是长时程增强（LTP），它在特定的突触活动模式后发生。我们提供的证据表明，L1细胞质结构域内YRSL基序的Y1176在LTP诱导的海马体中发生去磷酸化。去磷酸化的L1与AP-2和AP180相关联，而AP-2和AP180是网格蛋白介导的L1内化所必需的。这些数据表明，某些类型的神经活动可增强突触前位点网格蛋白介导的L1循环利用，且LTP诱导的突触变化的维持受L1循环利用的调节。
