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Importin α5 通过 MeCP2 和鞘氨醇激酶 1 调节焦虑。

Importin α5 Regulates Anxiety through MeCP2 and Sphingosine Kinase 1.

机构信息

Department of Biomolecular Sciences, Weizmann Institute of Science, Rehovot 76100, Israel.

Sagol School of Neuroscience, Tel Aviv University, Tel Aviv 69978, Israel.

出版信息

Cell Rep. 2018 Dec 11;25(11):3169-3179.e7. doi: 10.1016/j.celrep.2018.11.066.

Abstract

Importins mediate transport from synapse to soma and from cytoplasm to nucleus, suggesting that perturbation of importin-dependent pathways should have significant neuronal consequences. A behavioral screen on five importin α knockout lines revealed that reduced expression of importin α5 (KPNA1) in hippocampal neurons specifically decreases anxiety in mice. Re-expression of importin α5 in ventral hippocampus of knockout animals increased anxiety behaviors to wild-type levels. Hippocampal neurons lacking importin α5 reveal changes in presynaptic plasticity and modified expression of MeCP2-regulated genes, including sphingosine kinase 1 (Sphk1). Knockout of importin α5, but not importin α3 or α4, reduces MeCP2 nuclear localization in hippocampal neurons. A Sphk1 blocker reverses anxiolysis in the importin α5 knockout mouse, while pharmacological activation of sphingosine signaling has robust anxiolytic effects in wild-type animals. Thus, importin α5 influences sphingosine-sensitive anxiety pathways by regulating MeCP2 nuclear import in hippocampal neurons.

摘要

importins 介导从突触到胞体以及从细胞质到细胞核的运输,这表明 importin 依赖性途径的扰动应该对神经元有重大影响。对五个 importin α 敲除系的行为筛选表明,海马神经元中 importin α5(KPNA1)的表达减少特异性地降低了小鼠的焦虑。在敲除动物的腹侧海马中重新表达 importin α5 将焦虑行为增加到野生型水平。缺乏 importin α5 的海马神经元显示出突触前可塑性的变化和 MeCP2 调节基因的表达改变,包括鞘氨醇激酶 1(Sphk1)。importin α5 的敲除,而不是 importin α3 或 α4 的敲除,减少了海马神经元中 MeCP2 的核定位。Sphk1 阻断剂可逆转 importin α5 敲除小鼠的焦虑缓解,而鞘氨醇信号的药理学激活在野生型动物中具有强大的抗焦虑作用。因此,importin α5 通过调节海马神经元中 MeCP2 的核输入来影响鞘氨醇敏感的焦虑途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcb5/6302549/b00155d59bcf/fx1.jpg

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