EphB2 mediates social isolation-induced memory forgetting.

EphB2 mediates social isolation-induced memory forgetting.
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EphB2介导社会隔离引起的记忆遗忘

DOI:
10.1038/s41398-020-01051-6
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发表时间:
2020-11-09
影响因子:
6.8
通讯作者:
Sun S
Sun S
中科院分区:
医学1区
文献类型:
--
作者:
Wu XR;Zhang Y;Liu XD;Han WB;Xu NJ;Sun S

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青春期的社会孤立导致持久的缺陷,包括情绪和认知失调。然而,目前尚不清楚社会隔离如何影响某些记忆过程,以及涉及哪些分子机制。在本研究中,我们发现,在断奶后的社会隔离期间,导致长期的恐惧记忆的遗忘,这是由于下调海马CA1区的突触功能,EphB2,一个受体酪氨酸激酶,参与谷氨酸受体多蛋白复合物。病毒介导的EphB2敲低在CA 1模仿组圈养小鼠的记忆缺陷,而恢复EphB2的病毒过表达或resocialization逆转了记忆衰退在隔离的小鼠。综上所述,我们的发现表明,社交孤立通过破坏EphB2介导的突触可塑性而引起记忆遗忘,这可能为预防社交孤立或孤独引起的记忆丧失提供潜在的靶点。
Social isolation in adolescence leads to lasting deficits, including emotional and cognitive dysregulation. It remains unclear, however, how social isolation affects certain processes of memory and what molecular mechanisms are involved. In this study, we found that social isolation during the post-weaning period resulted in forgetting of the long-term fear memory, which was attributable to the downregulation of synaptic function in the hippocampal CA1 region mediated by EphB2, a receptor tyrosine kinase which involves in the glutamate receptor multiprotein complex. Viral-mediated EphB2 knockdown in CA1 mimicked the memory defects in group-housed mice, whereas restoration of EphB2 by either viral overexpression or resocialization reversed the memory decline in isolated mice. Taken together, our finding indicates that social isolation gives rise to memory forgetting by disrupting EphB2-mediated synaptic plasticity, which may provide a potential target for preventing memory loss caused by social isolation or loneliness.
多个EPHB受体酪氨酸激酶在海马中塑造树突状刺。
DOI: 10.1083/jcb.200306033
发表时间: 2003-12-22
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