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首页> 外文期刊>The European Journal of Neuroscience >Different responsiveness of striatonigral and striatopallidal neurons to L-DOPA after a subchronic intermittent L-DOPA treatment.
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Different responsiveness of striatonigral and striatopallidal neurons to L-DOPA after a subchronic intermittent L-DOPA treatment.

机译：亚慢性间歇性L-DOPA治疗后，纹状体神经和纹状体神经元对L-DOPA的反应不同。

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Abstract Early gene induction by L-DOPA in the striatum of dopamine denervated rats represents a useful way to study long-term modifications produced by this drug. The effects of acute and subchronic L-DOPA administration on zif-268 mRNA expression were compared in 6-hydroxydopamine-lesioned rats. Rats received a subchronic intermittent L-DOPA (6 mg/kg) treatment, which produces behavioural sensitization, a correlate of dyskinetic movements. Three days after interruption of subchronic treatment, zif-268 mRNA was evaluated after an L-DOPA challenge. Zif-268 mRNA levels increased in the lesioned dorsolateral striatum after either acute or subchronic L-DOPA administration. Double labelling of striatal cells with zif-268 and enkephalin or dynorphin mRNA probes was performed to assess neuronal activation in the indirect and direct output pathway. Single acute L-DOPA significantly increased zif-268 in all striatal neurons reflecting a hyperresponsiveness of dopamine-depleted striatum. After subchronic L-DOPA, zif-268 mRNA labelling was still increased in the striatonigral pathway, limited to dynorphin(+) neurons, whereas in all other neurons it was similar to the control value. Results suggest that striatal neurons responding to acute L-DOPA differ from those responding to subchronic L-DOPA. L-DOPA-induced behavioural sensitization was associated to a down-regulation in the responsiveness of striatopallidal and striatonigral dynorphin(-) neurons, whereas in striatonigral neurons containing dynorphin a hyperresponsiveness to L-DOPA was observed. High levels of zif-268, together with a persistent hyperresponsiveness of striatonigral dymorphinergic neurons and hyporesponsiveness of striatopallidal neurons, by creating an unbalanced state of striatal efferent neurons, may be implicated in dyskinetic movements observed in Parkinson's disease (PD).
机译：摘要L-DOPA在多巴胺失神经大鼠纹状体中早期诱导基因表达，是研究该药物产生的长期修饰的有效途径。比较了6-羟基多巴胺损伤大鼠的急性和亚慢性L-DOPA给药对zif-268 mRNA表达的影响。大鼠接受亚慢性间歇性L-DOPA（6 mg / kg）治疗，产生行为敏化，这是运动障碍运动的相关因素。亚慢性治疗中断三天后，在L-DOPA攻击后评估zif-268 mRNA。急性或亚慢性L-DOPA给药后，病变的背外侧纹状体中Zif-268 mRNA水平升高。用zif-268和脑啡肽或强啡肽mRNA探针对纹状体细胞进行了双重标记，以评估间接和直接输出途径中的神经元激活。单个急性L-DOPA在所有纹状体神经元中均显着增加zif-268，反映出多巴胺消耗的纹状体有高反应性。在亚慢性L-DOPA后，纹状体回合途径中的zif-268 mRNA标记仍增加，仅限于强啡肽（+）神经元，而在所有其他神经元中，其与对照值相似。结果表明，对急性L-DOPA有反应的纹状体神经元与对亚慢性L-DOPA有反应的纹状体神经元不同。 L-DOPA诱导的行为敏化与纹状体顶神经和纹状体神经强啡肽（-）神经元的反应性下调相关，而在含有强啡肽的纹状体神经元中，观察到对L-DOPA的高反应性。通过产生不平衡状态的纹状体传出神经元状态，高水平的zif-268以及持续存在的纹状体神经元吗啡能神经元的高反应性和纹状体神经节神经元的低反应性，可能与帕金森氏病（PD）中观察到的运动障碍运动有关。

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