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首页> 外文期刊>Behavioural Brain Research: An International Journal >Effects of blocking the dopamine biosynthesis and of neurotoxic dopamine depletion with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on voluntary wheel running in mice.
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Effects of blocking the dopamine biosynthesis and of neurotoxic dopamine depletion with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on voluntary wheel running in mice.

机译：1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）阻断多巴胺生物合成和神经毒性多巴胺耗竭对小鼠自主轮转的影响。

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In Parkinson's disease (PD) compensatory mechanisms such as an increase of the de novo biosynthesis of dopamine (DA) are thought to delay the onset of motor impairment. Here, we investigated whether the tyrosine hydroxylase (TH) inhibitor alpha-methyl-para-tyrosine (AMPT) affects behavioral deficits in the running wheel activity induced by the selective dopaminergic neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Immediately after MPTP treatment C57bl/6 mice showed reduced running wheel activity which lasted during the entire active phase (20:00 to 08:00h), recovered to baseline levels in the following 2 days and remained stable up to the end of the experiment. AMPT challenge significantly reduced wheel running activity in MPTP-treated mice in the first 3h after treatment. Post mortem HPLC analysis detected mean striatal DA levels in [Formula: see text] and [Formula: see text] -treated mice of 14.32 and 9.83ng/mg, respectively and in [Formula: see text] and [Formula: see text] -treated mice of 1.73 and 0.69ng/mg, respectively. Taken together, de novo biosynthesis of DA is a crucial component of the compensatory mechanisms which contributes to masking long-term behavioral deficits in the MPTP mouse model. Additionally, wheel running activity might provide a useful tool to study MPTP-induced behavioral deficits, shifts in circadian rhythmicity, and further compensatory mechanisms relevant to PD.
机译：在帕金森氏病（PD）中，诸如多巴胺（DA）的从头生物合成增加的代偿机制被认为会延迟运动障碍的发作。在这里，我们研究了酪氨酸羟化酶（TH）抑制剂α-甲基-对-酪氨酸（AMPT）是否会影响由选择性多巴胺能神经毒素1-甲基-4-苯基-1,2,3诱导的转轮活动中的行为缺陷， 6-四氢吡啶（MPTP）。 MPTP处理后，C57bl / 6小鼠立即表现出运转轮活动减少，该活动持续于整个活动阶段（20:00至08：00h），并在接下来的2天恢复到基线水平，并在实验结束前保持稳定。在治疗后的前3小时，AMPT攻击显着降低了MPTP处理的小鼠的滚轮行驶活动。验尸HPLC分析在[配方：参见文本]和[配方：参见文本]处理的小鼠中分别检测到平均纹状体DA水平为14.32和9.83ng / mg，在[配方：参见文本]和[配方：参见文本] -治疗的小鼠分别为1.73和0.69ng / mg。综上所述，DA的从头生物合成是补偿机制的重要组成部分，该机制有助于掩盖MPTP小鼠模型中的长期行为缺陷。此外，轮转活动可能会提供有用的工具来研究MPTP引起的行为缺陷，昼夜节律的变化以及与PD相关的其他补偿机制。

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