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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Protective effect of melatonin on 3-NP induced striatal interneuron injury in rats.
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Protective effect of melatonin on 3-NP induced striatal interneuron injury in rats.

机译：褪黑素对3-NP诱导的大鼠纹状体中间神经元损伤的保护作用。

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摘要

To confirm the effect of melatonin on 3-nitropropionic acid (3-NP)-induced striatal interneuron injury in rats, behavioral test, histology, immunohistochemistry and Western blotting were respectively used to characterize the behavioral changes of experimental animals in motor and cognition, the morphological changes of striatal interneurons and the expression level of protein markers induced by 3-NP. The results showed that (1) 3-NP induced dysfunction of experimental animals in movement, motor coordination and cognition could be relieved by melatonin treatment; (2) The 3-NP-induced lesion area was unvaryingly in dorsolateral striatum, with almost all neuronal loss in the lesion core, however, lots of neurons survived after melatonin treatment; (3) Immunohistochemical staining of the four interneuron types (parvalbuminergic, cholinergic, calretinergic, and neuropeptide Y-neuronal nitric oxide synthase co-containing) showed that, in the lesion core of 3-NP group, loss of the four interneuron types was obvious, but in transition zone, the processes and varicosities of calretinergic, and neuropeptide Y-neuronal nitric oxide synthase co-containing interneurons increased significantly. Melatonin treatment reduced the loss of the four interneuron types in the lesion core, and inhibited the increase of processes and varicosities in the transition zone; (4) Consistent with above results, the expression level of five interneuron protein markers were significantly increased in the striatum after melatonin treatment. Notably, in both the transition zone and the lesion core induced by 3-NP, TUNEL-positive cells were detected, but decreased significantly after melatonin treatment. The present results indicate that melatonin effectively protects the striatal neurons against the injury induced by 3-NP in rats.
机译：为证实褪黑素对3-硝基丙酸（3-NP）诱导的大鼠纹状体中间神经元损伤的作用，分别通过行为测试，组织学，免疫组化和Western blotting表征实验动物在运动和认知方面的行为变化， 3-NP诱导纹状体中间神经元的形态学改变和蛋白质标志物的表达水平结果表明：（1）褪黑素治疗可减轻3-NP诱导的实验动物运动，运动协调和认知功能障碍; （2）3-NP所致的病变区域在背外侧纹状体中无变化，病变核心几乎全部神经元丢失，但是，褪黑激素治疗后，许多神经元得以存活。 （3）四种中间神经元类型（小白蛋白能，胆碱能，钙视网膜蛋白能和神经肽Y-神经元一氧化氮合酶）的免疫组织化学染色显示，在3-NP组的病灶核心中，四种中间神经元类型的损失明显，但在过渡区，钙视蛋白能和神经肽Y-神经元一氧化氮合酶共含中间神经元的过程和曲度明显增加。褪黑素治疗减少了病变核中四种中间神经元类型的损失，并抑制了过渡区过程和静脉曲张的增加。 （4）与上述结果一致，褪黑激素处理后纹状体中5种中间神经元蛋白标志物的表达水平明显升高。值得注意的是，在3-NP诱导的过渡区和病变核心中，都检测到了TUNEL阳性细胞，但是在褪黑激素处理后，TUNEL阳性细胞明显减少。目前的结果表明褪黑激素有效保护纹状体神经元免受3-NP诱导的大鼠损伤。

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