Quantification of reserve pool dopamine in methionine sulfoxide reductase A null mice.
Quantification of reserve pool dopamine in methionine sulfoxide reductase A null mice.
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DOI：
10.1016/j.neuroscience.2011.01.001
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发表时间：
2011-03-17
期刊：
影响因子：
3.3
通讯作者：
Johnson MA
中科院分区：
文献类型：
--
作者：
Ortiz AN;Oien DB;Moskovitz J;Johnson MA
甲基亚砜还原酶A基因敲除（MsrA−/−）小鼠，作为一个潜在的模型，神经退行性疾病，遭受增加的氧化应激，以前已经发现有慢性脑多巴胺含量水平相对于对照小鼠升高。此外，这些高水平平行增加突触前多巴胺释放。在这项工作中，在碳纤维微电极上的快速扫描循环伏安法被用来定量敲除小鼠和野生型对照小鼠的纹状体储备池多巴胺。在α-甲基-p-酪氨酸（一种多巴胺合成抑制剂）存在下，在基因敲除小鼠和野生型小鼠的脑切片中测量安非他明诱导的储备池多巴胺流出。此外，测量了可卡因动员的储备池多巴胺的刺激释放。两个外排和刺激释放测量增强了从敲除小鼠的切片，这表明这些小鼠有更大的储备池多巴胺商店比野生型，这些商店被有效地动员。此外，多巴胺转运蛋白标记数据表明，在测量多巴胺流出的差异可能不是由改变多巴胺转运蛋白的表达。此外，来自MsrA−/−和野生型小鼠的切片对细胞外钙浓度的增加同样敏感，这表明钙进入或细胞内钙处理的潜在差异与储备池多巴胺释放增加无关。总的来说，这些结果表明，MsrA−/−敲除小鼠比野生型对照小鼠保持更大的多巴胺储备库，并且该库易于动员。
Methionine sulfoxide reductase A knockout (MsrA−/−) mice, which serve as a potential model for neurodegeneration, suffer from increased oxidative stress and have previously been found to have chronically elevated brain dopamine content levels relative to control mice. Additionally, these high levels parallel increased presynaptic dopamine release. In this work, fast-scan cyclic voltammetry at carbon-fiber microelectrodes was used to quantify striatal reserve pool dopamine in knockout mice and wild-type control mice. Reserve pool dopamine efflux, induced by amphetamine, was measured in brain slices from knockout and wild type mice in the presence of α-methyl-p-tyrosine, a dopamine synthesis inhibitor. Additionally, the stimulated release of reserve pool dopamine, mobilized by cocaine, was measured. Both efflux and stimulated release measurements were enhanced in slices from knockout mice, suggesting that these mice have greater reserve pool dopamine stores than wild-type and that these stores are effectively mobilized. Moreover, dopamine transporter labeling data indicate that the difference in measured dopamine efflux was likely not caused by altered dopamine transporter protein expression. Additionally, slices from MsrA−/− and wild-type mice were equally responsive to increasing extracellular calcium concentrations, suggesting that potential differences in either calcium entry or intracellular calcium handling are not responsible for increased reserve pool dopamine release. Collectively, these results demonstrate that MsrA−/− knockout mice maintain a larger dopamine reserve pool than wild-type control mice, and that this pool is readily mobilized.
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