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首页> 外文期刊>The Korean Journal of Physiology & Pharmacology >Mind Bomb-2 Regulates Hippocampus-dependent Memory Formation and Synaptic Plasticity
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Mind Bomb-2 Regulates Hippocampus-dependent Memory Formation and Synaptic Plasticity

机译：心灵炸弹2调节海马依赖的记忆形成和突触可塑性。

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Notch signaling is a key regulator of neuronal fate during embryonic development, but its function in the adult brain is still largely unknown. Mind bomb-2 (Mib2) is an essential positive regulator of the Notch pathway, which acts in the Notch signal-sending cells. Therefore, genetic deletion of Mib2 in the mouse brain might help understand Notch signaling-mediated cell-cell interactions between neurons and their physiological function. Here we show that deletion of Mib2 in the mouse brain results in impaired hippocampal spatial memory and contextual fear memory. Accordingly, we found impaired hippocampal synaptic plasticity in Mib2 knock-out (KO) mice; however, basal synaptic transmission did not change at the Schaffer collateral-CA1 synapses. Using western blot analysis, we found that the level of cleaved Notch1 was lower in Mib2 KO mice than in wild type (WT) littermates after mild foot shock. Taken together, these data suggest that Mib2 plays a critical role in synaptic plasticity and spatial memory through the Notch signaling pathway.
机译：Notch信号是胚胎发育过程中神经元命运的关键调节因子，但其在成人大脑中的功能仍然未知。心理炸弹2（Mib2）是Notch通路的重要正调控因子，它在Notch信号发送细胞中起作用。因此，小鼠大脑中Mib2的基因缺失可能有助于理解Notch信号介导的神经元之间的细胞间相互作用及其生理功能。在这里，我们显示小鼠大脑中Mib2的缺失会导致海马空间记忆和上下文恐惧记忆受损。因此，我们发现Mib2基因敲除（KO）小鼠海马突触可塑性受损。然而，在Schaffer侧支CA1突触中，基础突触传递没有改变。使用蛋白质印迹分析，我们发现轻度足部休克后，Mib2 KO小鼠的Notch1裂解水平低于野生型（WT）同窝仔。综上所述，这些数据表明，Mib2通过Notch信号通路在突触可塑性和空间记忆中起关键作用。

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