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作 者:Menghan Dai Jie Li Xiangwen Hao Na Li Mingfang Zheng Miao He Yu Gu
出 处:《Neuroscience Bulletin》2024年第9期1245-1260,共16页神经科学通报(英文版)
基 金:National Natural Science Foundation of China(31872764 and 82171090);Shanghai Science and Technology Committee Rising-Star Program(19QA1401600);Shanghai Municipal Science and Technology Major Project(2018SHZDZX01);ZJLab,Shanghai Center for Brain Science and Brain-Inspired Technology.
摘 要:Abnormal visual experience during the critical period can cause deficits in visual function,such as amblyopia.High magnesium(Mg^(2+))supplementary can restore ocular dominance(OD)plasticity,which promotes the recovery of amblyopic eye acuity in adults.However,it remains unsolved whether Mg^(2+)could recover binocular vision in amblyopic adults and what the molecular mechanism is for the recovery.We found that in addition to the recovery of OD plasticity,binocular integration can be restored under the treatment of high Mg^(2+)in amblyopic mice.Behaviorally,Mg^(2+)-treated amblyopic mice showed better depth perception.Moreover,the effect of high Mg^(2+)can be suppressed with transient receptor potential melastatin-like 7(TRPM7)knockdown.Collectively,our results demonstrate that high Mg^(2+)could restore binocular visual functions from amblyopia.TRPM7 is required for the restoration of plasticity in the visual cortex after high Mg^(2+)treatment,which can provide possible clinical applications for future research and treatment of amblyopia.
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