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首页> 外文期刊>Hippocampus >Pyridoxal-5'-phosphate phosphatase/chronophin inhibits long-term potentiation induction in the rat dentate gyrus.
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Pyridoxal-5'-phosphate phosphatase/chronophin inhibits long-term potentiation induction in the rat dentate gyrus.

机译:吡rid醛-5'-磷酸磷酸酶/计时蛋白抑制大鼠齿状回的长期增强诱导作用。

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摘要

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.
机译:吡rid醛5'-磷酸(PLP)-磷酸酶/计时蛋白(PLPP / CIN)直接使肌动蛋白解聚因子(ADF)/ cofilin以及PLP脱磷酸化。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,但没有直接证据支持长期增强(LTP)诱导过程中PLPP / CIN与F-肌动蛋白聚合之间的相关性。在这项研究中,我们调查了LTP诱导后PLPP / CIN的表达是否改变,以及Tat-PLPP / CIN的转导是否影响大鼠齿状回(DG)的LTP诱导。 LTP诱导后,齿状颗粒细胞的PLPP / CIN免疫反应性明显降低。与盐水或经Tat蛋白处理的动物相比,Tat-PLPP / CIN转导(20和200 microg / kg)降低了高频刺激诱导的群体尖峰振幅增强的效率。 PLPP / CIN蛋白水平与磷酸化ADF / cofilin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的海马形态学特征(树突棘重组)的变化中起重要作用。

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