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首页> 外文期刊>The European Journal of Neuroscience >Concomitant short- and long-duration response to levodopa in the 6-OHDA-lesioned rat: a behavioural and molecular study.
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Concomitant short- and long-duration response to levodopa in the 6-OHDA-lesioned rat: a behavioural and molecular study.

机译：在6-OHDA损伤大鼠中对左旋多巴同时发生的短期和长期反应：一项行为和分子研究。

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摘要

The long-duration response (LDR) is a sustained improvement in parkinsonism due to chronic levodopa therapy and lasts after discontinuation of treatment. We have investigated the molecular changes that underlie the LDR in rats with a unilateral 6-hydroxydopamine (6-OHDA) lesion. Animals were treated for 22 days with levodopa or saline. Forelimb akinesia was evaluated prior and following a test dose of levodopa. Rotational behaviour was weekly evaluated. Levodopa induced an improvement in the parkinsonian limb akinesia that lasted for 48 h after withdrawal. A shortening in the duration of rotational behaviour was observed. After 3 days of washout, levodopa treatment maintained elevated striatal preproenkephalin mRNA expression, also inducing an increase in preprodynorphin (PDyn) and dopamine D-3 receptor mRNAs, but without any modification of the adenosine A(2A) mRNA expression induced by 6-OHDA. Levodopa reversed the lesion-induced increase in the expression of cytochrome oxidase mRNA in the subthalamic nucleus and glutamate decarboxylase mRNA in the pars reticulata of the substantia nigra. After 7 days of levodopa washout, the molecular markers show a decline in the basal ganglia evolving towards the parkinsonian state, being statistically significant for the striatal PDyn mRNA. This study characterizes the concomitant presence of the short-duration response and LDR to levodopa in the 6-OHDA model of parkinsonism and shows that the molecular changes induced by levodopa in the basal ganglia are not permanent and that this reversal after levodopa washout may be responsible for the gradual motor deterioration that characterize the LDR.
机译：长期反应（LDR）是由于慢性左旋多巴疗法导致的帕金森综合症的持续改善，并在停药后持续。我们研究了单侧6-羟基多巴胺（6-OHDA）损伤大鼠LDR的分子变化。用左旋多巴或盐水治疗动物22天。在测试剂量的左旋多巴之前和之后评估前肢运动障碍。每周评估旋转行为。左旋多巴导致帕金森病肢体运动障碍改善，停药后持续48小时。观察到旋转行为持续时间的缩短。冲洗3天后，左旋多巴治疗维持纹状体前脑啡肽原mRNA表达升高，也诱导前强啡肽（PDyn）和多巴胺D-3受体mRNA的增加，但未对6-OHDA诱导的腺苷A（2A）mRNA表达进行任何修饰。 。左旋多巴逆转了病灶诱导的丘脑下丘脑核中细胞色素氧化酶mRNA表达的增加和黑质旁壁的谷氨酸脱羧酶mRNA的表达增加。左旋多巴冲洗7天后，分子标记显示基底神经节向帕金森病状态下降，对纹状体PDyn mRNA具有统计学意义。这项研究的特点是在帕金森病6-OHDA模型中同时存在左旋多巴的短期反应和LDR，并表明左旋多巴在基底神经节中引起的分子变化不是永久性的，左旋多巴冲洗后的这种逆转可能是造成这种情况的原因。 LDR的特征是电机逐渐退化。

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