Synaptic vesicle glycoprotein 2C enhances vesicular storage of dopamine and counters dopaminergic toxicity

Dopaminergic neurons of the substantia nigra exist in a persistent state of vulnerability resulting from high baseline oxidative stress, high energy demand, and broad unmyelinated axonal arborizations. Impairments in the storage of dopamine compound this stress due to cytosolic reactions that transform the vital neurotransmitter into an endogenous neurotoxicant, and this toxicity is thought to contribute to the dopamine neuron degeneration that occurs Parkinson’s disease. We have previously identified synaptic vesicle glycoprotein 2C (SV2C) as a modifier of vesicular dopamine function, demonstrating that genetic ablation of SV2C in mice results in decreased dopamine content and evoked dopamine release in the striatum. Here, we adapted a previously published in vitro assay utilizing false fluorescent neurotransmitter 206 (FFN206) to visualize how SV2C regulates vesicular dopamine dynamics and identified that SV2C promotes the uptake and retention of FFN206 within vesicles. In addition, w..., , , # Synaptic vesicle glycoprotein 2C enhances vesicular storage of dopamine and counters dopaminergic toxicity

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This dataset contains the raw data corresponding to the manuscript Synaptic vesicle glycoprotein 2C enhances vesicular storage of dopamine and counters dopaminergic toxicity. Inclusive in this dataset is the following: 1) a GraphPad Prism file containing all of the data found in the manuscript with statistical analysis and graphs; 2) individual .csv files containing the data for each graph of data found in the manuscript including a separate .csv for corresponding statistics (files ending in \_stats); 3) individual PDFs of graphs generated in GraphPad Prism; and 4) raw image files for microscopy and Western blots. These data demonstrate the principal findings for the manuscript that the protein SV2C: 1) enhances vesicular storage of dopamine and dopamine analogues (e.g., FFN206 and MPP+), and 2) confers neuroprotection against dopaminergic toxicity.

## Description of the d...

黑质多巴胺能神经元因高基础氧化应激、高能量需求以及广泛的无髓鞘轴突分支而持续处于易损状态。多巴胺储存障碍会因胞质反应将该关键神经递质转化为内源性神经毒素而加重上述应激，这种毒性被认为与帕金森病（Parkinson’s disease）中发生的多巴胺神经元变性密切相关。我们此前已鉴定出突触囊泡糖蛋白2C（synaptic vesicle glycoprotein 2C, SV2C）作为囊泡多巴胺功能的调控因子，证实小鼠中SV2C的基因敲除会导致纹状体多巴胺含量降低以及诱发的多巴胺释放减少。本研究优化了此前发表的利用假荧光神经递质206（false fluorescent neurotransmitter 206, FFN206）的体外实验体系，以探究SV2C如何调控囊泡多巴胺动力学，并发现SV2C可促进FFN206在囊泡内的摄取与滞留。此外，……
# 突触囊泡糖蛋白2C增强多巴胺的囊泡储存并对抗多巴胺能毒性

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本数据集包含与论文《突触囊泡糖蛋白2C增强多巴胺的囊泡储存并对抗多巴胺能毒性》相对应的原始实验数据。本数据集涵盖以下内容：1）包含论文中全部数据、统计分析结果及对应图表的GraphPad Prism文件；2）对应论文中每张图表数据的独立.csv文件，其中包含用于统计分析的单独.csv文件（文件名以_stats结尾）；3）由GraphPad Prism生成的图表的独立PDF文件；4）显微镜成像与蛋白质印迹（Western blots）的原始图像文件。上述数据验证了该论文的核心发现：蛋白SV2C可实现以下功能：1）增强多巴胺及其类似物（如FFN206与MPP+）的囊泡储存能力；2）赋予神经元对抗多巴胺能毒性的神经保护作用。

## 数据集描述（d...）