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首页> 外文期刊>Journal of Behavioral and Brain Science >The Time Course of D1 Agonist Induced Striatonigral ERK1/2 Signaling in a Rat Model of Parkinson’s Disease
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The Time Course of D1 Agonist Induced Striatonigral ERK1/2 Signaling in a Rat Model of Parkinson’s Disease

机译：D1激动剂诱导帕金森病大鼠模型中纹状体ERK1 / 2信号传导的时程

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Using a rat model of hemiparkinsonism, we examined the time-course of D1 agonist, SKF-38393-induced changes in extracellular signaling regulated kinases 1/2 (ERK1/2) phosphorylation in the striatum and substantia nigra (SN). We unilaterally lesioned the rat median forebrain bundle with 6-hydroxydopamine. Dopaminergic lesioned rats were administered with SKF-38393 and perfused at 15, 30, 60, or 120 minutes after the drug. Immunohistochemical analysis of striatum and SN revealed, as expected, a loss of tyrosine hydroxylase and a decrease of substance P in lesioned rats. SKF-38393 induced a robust increase in phospho-ERK1/2 levels in the lesioned striatum, which peaked at 15 min and substantially declined by 120 min. We report for the first time that similar changes were observed in the SN. The time-dependent ERK 1/2 activation in the striatonigral neurons may play a role in the therapeutic and/or side effects such as dyskinesias related to the dopamine agonist treatment for Parkinson’s disease.
机译：我们使用大鼠半帕金森病模型，研究了D1激动剂的时程，SKF-38393诱导纹状体和黑质（SN）中细胞外信号调节激酶1/2（ERK1 / 2）磷酸化的变化。我们单方面用6-羟基多巴胺损伤大鼠中脑前束。给多巴胺能损伤的大鼠施用SKF-38393，并在用药后15、30、60或120分钟进行灌注。纹状体和SN的免疫组织化学分析显示，正如所预期的，病变大鼠中酪氨酸羟化酶的损失和P物质的减少。 SKF-38393引起病变纹状体中磷酸化-ERK1 / 2水平的强烈增加，在15分钟达到峰值，到120分钟时大幅下降。我们首次报告在SN中观察到类似的变化。纹状体神经元神经元的时间依赖性ERK 1/2激活可能在治疗和/或副作用中发挥作用，例如与帕金森氏病多巴胺激动剂治疗有关的运动障碍。

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