PDZ proteins interacting with C-terminal GluR2/3 are involved in a PKC-dependent regulation of AMPA receptors at hippocampal synapses
PDZ proteins interacting with C-terminal GluR2/3 are involved in a PKC-dependent regulation of AMPA receptors at hippocampal synapses
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DOI：
10.1016/s0896-6273(00)00160-4
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发表时间：
2000-12-01
期刊：
影响因子：
16.2
通讯作者：
Isaac, JTR
中科院分区：
文献类型：
--
作者：
Daw, MI;Chittajallu, R;Isaac, JTR
我们研究了PDZ蛋白（GRIP，ABP和PICK 1）与C-末端GluR 2相互作用的作用，通过使用全细胞记录将ct-GluR 2肽（“pep 2-SVKI”）注入海马切片中的CA 1锥体神经元。Pep 2-SVKI，但不是一个控制或PICK 1选择性肽，导致AMPAR介导的EPSC振幅增加约三分之一的控制神经元和大多数神经元后，以前的诱导LTD。Pep 2-SVKI也阻止LTD，但是，这发生在所有的神经元。PKC抑制剂防止pep 2-SVKI对突触传递和LTD的这些影响。我们提出了一个模型，其中LTD的维护涉及AMPAR与PDZ蛋白的结合，以防止其重新插入。我们还提供了PKC在去抑郁症过程中调节AMPAR重新插入的证据。
We investigated the role of PDZ proteins (GRIP, ABP, and PICK1) interacting with the C-terminal GluR2 by infusing a ct-GluR2 peptide ("pep2-SVKI") into CA1 pyramidal neurons in hippocampal slices using whole-cell recordings. Pep2-SVKI, but not a control or PICK1 selective peptide, caused AMPAR-mediated EPSC amplitude to increase in approximately one-third of control neurons and in most neurons following the prior induction of LTD. Pep2-SVKI also blocked LTD; however, this occurred in all neurons. A PKC inhibitor prevented these effects of pep2-SVKI on synaptic transmission and LTD. We propose a model in which the maintenance of LTD involves the binding of AMPARs to PDZ proteins to prevent their reinsertion. We also present evidence that PKC regulates AMPAR reinsertion during dedepression.