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吡哆醛-5'-磷酸酶/生物钟蛋白抑制大鼠齿状回长时程增强诱导。

Pyridoxal-5'-phosphate phosphatase/chronophin inhibits long-term potentiation induction in the rat dentate gyrus.

机构信息

Department of Anatomy and Neurobiology, College of Medicine, Hallym University, Chunchon, Kangwon-Do, South Korea.

出版信息

Hippocampus. 2009 Nov;19(11):1078-89. doi: 10.1002/hipo.20568.

DOI:10.1002/hipo.20568
PMID:19253407
Abstract

Pyridoxal-5'-phosphate (PLP)-phosphatase/chronophin (PLPP/CIN) directly dephosphorylates actin-depolymerizing factor (ADF)/cofilin as well as PLP. Although PLPP/CIN plays a role in the regulation of F-actin and vitamin B(6) metabolism, there is no direct evidence to support a correlation between PLPP/CIN and F-actin polymerization during long-term potentiation (LTP) induction. In this study, we investigated whether the expression of PLPP/CIN is altered following LTP induction, and whether Tat-PLPP/CIN transduction affects LTP induction in the rat dentate gyrus (DG). PLPP/CIN immunoreactivity was markedly decreased in dentate granule cells after the induction of LTP. Tat-PLPP/CIN transduction (20 and 200 microg/kg) decreased the efficiency of high frequency stimulus-induced potentiation of populations spike amplitude as compared to saline or Tat-protein-treated animals. The PLPP/CIN protein level showed an inverse correlation with phosphorylated ADF/cofilin levels and F-actin content. These findings suggest that PLPP/CIN-mediated actin dynamics may play an important role in the changes of morphological properties (dendritic spine reorganization) of the hippocampus in LTP.

摘要

吡哆醛-5'-磷酸(PLP)-磷酸酶/chronophin(PLPP/CIN)可直接去磷酸化肌动蛋白解聚因子(ADF)/丝切蛋白以及 PLP。尽管 PLPP/CIN 在 F-肌动蛋白和维生素 B(6)代谢的调节中发挥作用,但没有直接证据表明 PLPP/CIN 与长时程增强(LTP)诱导期间的 F-肌动蛋白聚合之间存在相关性。在这项研究中,我们研究了 LTP 诱导后 PLPP/CIN 的表达是否发生改变,以及 Tat-PLPP/CIN 转导是否会影响大鼠齿状回(DG)中的 LTP 诱导。LTP 诱导后,齿状颗粒细胞中的 PLPP/CIN 免疫反应性明显降低。与盐水或 Tat-蛋白处理的动物相比,Tat-PLPP/CIN 转导(20 和 200 μg/kg)降低了高频刺激诱导的群体锋电位幅度增强的效率。PLPP/CIN 蛋白水平与磷酸化 ADF/丝切蛋白水平和 F-肌动蛋白含量呈负相关。这些发现表明,PLPP/CIN 介导的肌动蛋白动力学可能在 LTP 中海马体形态特性(树突棘重组)的变化中发挥重要作用。

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