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• W4386945895 abstract "Fear and anxiety are common in Parkinson’s disease (PD) and may be caused by pathologies outside the dopaminergic system. Increasing evidence has shown that alpha-synuclein (α-syn) is involved in the development of anxiety in PD. In this study, we examined the effects of α-syn nuclear translocation on anxiety-like behavior in mice by overexpressing α-syn in the nuclei of the cell in the hippocampus. Our results show that α-syn overexpression in the nuclei increased the excitability of hippocampal neurons and activated NG2 glial cells and promoted the synthesis and release of γ-aminobutyric acid (GABA). And nuclear localization of α-syn led to the loss of neurotrophic factors and decreased neurogenesis. Meanwhile, the hippocampus and amygdala acted synergistically, resulting in pathologic accumulation of α-syn and gliosis in the amygdala and caused loss of interneurons. These events led to the impairments of hippocampus and amygdala function, which ultimately induced anxiety-like behavior in mice. The findings obtained in our present study indicate that excessive nuclear translocation of α-syn in hippocampal neurons and damage to the amygdala circuits may be important in the development of anxiety in PD." @default.
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• W4386945895 date "2023-11-01" @default.
• W4386945895 modified "2023-10-07" @default.
• W4386945895 title "Nuclear localization of alpha-synuclein induces anxiety-like behavior in mice by decreasing hippocampal neurogenesis and pathologically affecting amygdala circuits" @default.
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• W4386945895 doi "https://doi.org/10.1016/j.neulet.2023.137490" @default.
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