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首页> 外文期刊>The European Journal of Neuroscience >Striatal-enriched protein tyrosine phosphatase (STEP) knockout mice have enhanced hippocampal memory.
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Striatal-enriched protein tyrosine phosphatase (STEP) knockout mice have enhanced hippocampal memory.

机译：纹状体富集的蛋白酪氨酸磷酸酶（STEP）敲除小鼠具有增强的海马记忆。

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Striatal-enriched protein tyrosine phosphatase (STEP) is a brain-specific phosphatase that opposes synaptic strengthening by the regulation of key synaptic signaling proteins. Previous studies suggest a possible role for STEP in learning and memory. To demonstrate the functional importance of STEP in learning and memory, we generated STEP knockout (KO) mice and examined the effect of deletion of STEP on behavioral performance, as well as the phosphorylation and expression of its substrates. Here we report that loss of STEP leads to significantly enhanced performance in hippocampal-dependent learning and memory tasks. In addition, STEP KO mice displayed greater dominance behavior, although they were normal in their motivation, motor coordination, visual acuity and social interactions. STEP KO mice displayed enhanced tyrosine phosphorylation of extracellular-signal regulated kinase 1/2 (ERK1/2), the NR2B subunit of the N-methyl-D-aspartate receptor (NMDAR) and proline-rich tyrosine kinase (Pyk2), as well as an increased phosphorylation of ERK1/2 substrates. Concomitant with the increased phosphorylation of NR2B, synaptosomal expression of NR1/NR2B NMDARs was increased in STEP KO mice, as was the GluR1/GluR2 containing alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptors (AMPARs), providing a potential molecular mechanism for the improved cognitive performance. The data support a role for STEP in the regulation of synaptic strengthening. The absence of STEP improves cognitive performance, and may do so by the regulation of downstream effectors necessary for synaptic transmission.
机译：纹状体富集的蛋白酪氨酸磷酸酶（STEP）是一种脑特异性磷酸酶，它通过调节关键的突触信号蛋白来反对突触增强。先前的研究表明，STEP在学习和记忆中可能发挥作用。为了证明STEP在学习和记忆中的功能重要性，我们生成了STEP基因敲除（KO）小鼠，并检查了STEP缺失对行为表现的影响，以及其底物的磷酸化和表达。在这里，我们报告说，STEP的丧失会导致海马依赖性学习和记忆任务的表现显着增强。此外，尽管STEP KO小鼠的动机，运动协调，视敏度和社交互动均正常，但它们表现出更大的主导行为。 STEP KO小鼠的胞外信号调节激酶1/2（ERK1 / 2），N-甲基-D-天冬氨酸受体（NMDAR）的NR2B亚基和富含脯氨酸的酪氨酸激酶（Pyk2）的酪氨酸磷酸化也增强作为ERK1 / 2底物磷​​酸化的增加。随着NR2B磷酸化的增加，NR1 / NR2B NMDAR的突触体表达在STEP KO小鼠中增加，GluR1 / GluR2包含α-氨基-3-羟基-5-甲基-4-异恶唑-丙酸受体（AMPAR） ），为提高认知能力提供了潜在的分子机制。数据支持STEP在突触增强调控中的作用。没有STEP可以提高认知能力，并且可以通过调节突触传递所必需的下游效应子来改善认知能力。

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