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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Protein phosphatase 1-dependent bidirectional synaptic plasticity controls ischemic recovery in the adult brain.
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Protein phosphatase 1-dependent bidirectional synaptic plasticity controls ischemic recovery in the adult brain.

机译：蛋白磷酸酶1依赖性双向突触可塑性控制成人大脑中的缺血性恢复。

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摘要

Protein kinases and phosphatases can alter the impact of excitotoxicity resulting from ischemia by concurrently modulating apoptotic/survival pathways. Here, we show that protein phosphatase 1 (PP1), known to constrain neuronal signaling and synaptic strength (Mansuy et al., 1998; Morishita et al., 2001), critically regulates neuroprotective pathways in the adult brain. When PP1 is inhibited pharmacologically or genetically, recovery from oxygen/glucose deprivation (OGD) in vitro, or ischemia in vivo is impaired. Furthermore, in vitro, inducing LTP shortly before OGD similarly impairs recovery, an effect that correlates with strong PP1 inhibition. Conversely, inducing LTD before OGD elicits full recovery by preserving PP1 activity, an effect that is abolished by PP1 inhibition. The mechanisms of action of PP1 appear to be coupled with several components of apoptotic pathways, in particular ERK1/2 (extracellular signal-regulated kinase 1/2) whose activation is increased by PP1 inhibition both in vitro and in vivo. Together, these results reveal that the mechanisms of recovery in the adult brain critically involve PP1, and highlight a novel physiological function for long-term potentiation and long-term depression in the control of brain damage and repair.
机译：蛋白激酶和磷酸酶可通过同时调节细胞凋亡/存活途径来改变缺血引起的兴奋性毒性的影响。在这里，我们显示已知可限制神经元信号传导和突触强度的蛋白磷酸酶1（PP1）（Mansuy等，1998; Morishita等，2001）可以严格调节成年大脑的神经保护途径。当PP1在药理或遗传学上受到抑制时，体外或体内缺血缺氧/葡萄糖剥夺（OGD）的恢复就会受到损害。此外，在体外，在OGD之前不久诱导LTP同样会损害恢复，这种作用与强烈的PP1抑制作用有关。相反，在OGD之前诱导LTD可以通过保留PP1活性来完全恢复，而PP1的抑制作用则消除了这种作用。 PP1的作用机制似乎与细胞凋亡途径的某些成分有关，特别是ERK1 / 2（细胞外信号调节激酶1/2），其活化在体外和体内都受到PP1抑制作用的增强。总之，这些结果表明，成年大脑的恢复机制关键涉及PP1，并突出了一种新的生理功能，可在控制脑部损伤和修复中长期增强和长期抑制抑郁。

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