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首页> 外文期刊>The European Journal of Neuroscience >Different phosphatase-dependent mechanisms mediate long-term depression and depotentiation of long-term potentiation in mouse hippocampal CA1 area.
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Different phosphatase-dependent mechanisms mediate long-term depression and depotentiation of long-term potentiation in mouse hippocampal CA1 area.

机译：不同的磷酸酶依赖性机制介导小鼠海马CA1区的长期抑制和长期增强。

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摘要

Two types of synaptic depression have been described in the hippocampus, long-term depression and depotentiation of long-term potentiation known to recruit the serine/threonine protein phosphatases PP1, PP2A and PP2B (calcineurin). The contribution of each of these protein phosphatases is controversial. To examine the role of the Ca2+/calmodulin-dependent protein phosphatase calcineurin in long-term depression and depotentiation, we analysed the effect of genetically inhibiting calcineurin reversibly in the hippocampus, using the doxycycline-dependent rtTA system in transgenic mice. We show that reducing calcineurin activity has no effect on long-term depression but reversibly affects depotentiation. Consistently, the calcineurin inhibitor FK-506 reproduces the depotentiation impairment observed in the mutant mice but does not affect long-term depression in control animals. In contrast, the PP1/PP2A inhibitor okadaic acid fully blocks both long-term depression and depotentiation. These data demonstratethat the nature of signalling cascades induced by synaptic activity depends on the initial synaptic state. While depression of potentiated synaptic responses requires activation of PP1/PP2A and/or calcineurin, depression of basal synaptic responses depends only on PP1/PP2A activation.
机译：海马中已经描述了两种类型的突触抑制，长期抑制和长期增强的去电位，已知其募集丝氨酸/苏氨酸蛋白磷酸酶PP1，PP2A和PP2B（钙调神经磷酸酶）。这些蛋白质磷酸酶的每一种的贡献是有争议的。为了检查Ca2 + /钙调蛋白依赖性蛋白磷酸酶钙调磷酸酶在长期抑郁和去势中的作用，我们使用了强力霉素依赖性rtTA系统在转基因小鼠中分析了可逆性抑制海马中钙调磷酸酶的作用。我们表明减少钙调神经磷酸酶活性对长期抑郁没有影响，但可逆地影响去势。一致地，钙调神经磷酸酶抑制剂FK-506重现了在突变小鼠中观察到的去势损伤，但不影响对照动物的长期抑郁。相反，PP1 / PP2A抑制剂冈田酸完全阻断了长期的抑郁和去势。这些数据证明由突触活性诱导的信号级联反应的性质取决于初始突触状态。抑制突触增强反应需要激活PP1 / PP2A和/或钙调神经磷酸酶，而抑制基础突触响应仅取决于PP1 / PP2A激活。

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