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碱性成纤维细胞生长因子对培养的中脑腹侧多巴胺能神经元中α-突触核蛋白的调控

Regulation of alpha-synuclein by bFGF in cultured ventral midbrain dopaminergic neurons.

作者信息

Rideout Hardy J, Dietrich Paula, Savalle Magali, Dauer William T, Stefanis Leonidas

机构信息

Department of Neurology, Columbia University, Black Building Room 326, 650 W. 168th Street, New York, NY 10032, USA.

出版信息

J Neurochem. 2003 Feb;84(4):803-13. doi: 10.1046/j.1471-4159.2003.01574.x.

Abstract

Alpha-synuclein is a neuronal protein that is implicated in the control of synaptic vesicle function and in Parkinson's disease (PD). Consequently, alterations of alpha-synuclein levels may play a role in neurotransmission and in PD pathogenesis. However, the factors that regulate alpha-synuclein levels are unknown. Growth factors mediate neurotrophic and plasticity effects in CNS neurons, and may play a role in disease states. Here we examine the regulation of alpha-synuclein levels in primary CNS neurons, with particular emphasis on dopaminergic neurons. E18 rat cortical neurons and dopaminergic neurons of E14 rat ventral midbrain showed an induction of alpha-synuclein protein levels with maturation in culture. Application of basic Fibroblast growth factor (bFGF) promoted alpha-synuclein expression selectively within dopaminergic, and not GABAergic or cortical neurons. This induction was blocked by actinomycin D, but not by inhibition of bFGF-induced glial proliferation. alpha-Synuclein levels were not altered by glial-derived neurotrophic factor (GDNF), or by apoptotic stimuli. We conclude that bFGF promotes alpha-synuclein expression in cultured ventral midbrain dopaminergic neurons through a direct transcriptional effect. These results suggest that distinct growth factors may thus mediate plasticity responses or influence disease states in ventral midbrain dopaminergic neurons.

摘要

α-突触核蛋白是一种神经元蛋白,与突触小泡功能的调控以及帕金森病(PD)有关。因此,α-突触核蛋白水平的改变可能在神经传递和PD发病机制中起作用。然而,调节α-突触核蛋白水平的因素尚不清楚。生长因子介导中枢神经系统(CNS)神经元的神经营养和可塑性效应,并可能在疾病状态中发挥作用。在此,我们研究了原代CNS神经元中α-突触核蛋白水平的调节,特别关注多巴胺能神经元。E18大鼠皮层神经元和E14大鼠腹侧中脑的多巴胺能神经元在培养过程中随着成熟而出现α-突触核蛋白水平的诱导。应用碱性成纤维细胞生长因子(bFGF)可选择性地促进多巴胺能神经元而非GABA能或皮层神经元中α-突触核蛋白的表达。这种诱导被放线菌素D阻断,但不受bFGF诱导的胶质细胞增殖抑制的影响。α-突触核蛋白水平不受胶质细胞源性神经营养因子(GDNF)或凋亡刺激的影响。我们得出结论,bFGF通过直接转录作用促进培养的腹侧中脑多巴胺能神经元中α-突触核蛋白的表达。这些结果表明,不同的生长因子可能因此介导腹侧中脑多巴胺能神经元的可塑性反应或影响疾病状态。

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