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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Behavioral effects of aminochrome and dopachrome injected in the rat substantia nigra.
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Behavioral effects of aminochrome and dopachrome injected in the rat substantia nigra.

机译：在大鼠黑质中注射氨基色素和多巴色素的行为效应。

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The exact mechanism of cell death in neurodegenerative diseases remains obscure, although there is evidence that their pathogenesis may involve the formation of free radicals originating from the oxidative metabolism of catecholamines. The purpose of this study was to evaluate the degree of neurodegenerative changes and behavioral impairments induced by unilateral injection into the rat substantia nigra of cyclized o-quinones, aminochrome and dopachrome, derived from oxidizing dopamine and L-DOPA, respectively, with Mn(3+)-pyrophosphate complex. The behavioral changes were compared with those induced after selective lesions of dopaminergic neurons with 6-hydroxydopamine (6-OHDA). Intranigral injection of aminochrome and dopachrome produced impairment in motor and cognitive behaviors. The behavioral impairment was also revealed by apomorphine-induced rotational asymmetry. Apomorphine (0.5 mg/kg sc) significantly increased rotational behavior in rats injected with aminochrome and dopachrome. These rats presented a clear motor bias showing a significant contralateral rotation activity, similar but less vigorous that in rats injected with 6-OHDA. The avoidance conditioning was seriously impaired in rats injected with aminochrome and dopachrome although only dopachrome-injected rats showed a similar hypomotility to 6-OHDA-injected rats. The behavioral effects were correlated to the extent of striatal tyrosine hydroxylase (TH)-positive fiber loss. Rats receiving unilateral intranigral aminochrome and dopachrome injections exhibited a 47.9+/-5.1% and a 39.7+/-4.4% reduction in nigrostriatal TH-positive fiber density. In conclusion, this study provided evidence that oxidizing DA and L-DOPA to cytotoxic quinones, aminochrome and dopachrome appears to be an important mediator of oxidative damage in vivo.
机译：神经退行性疾病中细胞死亡的确切机制仍然不清楚，尽管有证据表明它们的发病机理可能涉及源自儿茶酚胺氧化代谢的自由基的形成。这项研究的目的是评估分别从Mn（3）氧化多巴胺和L-DOPA衍生的环化邻醌，氨基色素和多巴色素分别向大鼠黑质中单侧注射所致的神经退行性改变和行为受损程度。 +）-焦磷酸盐配合物。将行为变化与用6-羟基多巴胺（6-OHDA）对多巴胺能神经元选择性损伤后诱发的行为变化进行比较。鼻内注射氨基色素和多巴色素会导致运动和认知行为受损。阿朴吗啡诱导的旋转不对称也揭示了行为障碍。阿扑吗啡（0.5 mg / kg sc）在注射氨基色素和多巴色素的大鼠中显着增加旋转行为。这些大鼠表现出明显的运动偏见，显示出显着的对侧旋转活动，与注射6-OHDA的大鼠相似但没有那么剧烈。尽管仅注射多巴色素的大鼠表现出与注射6-OHDA的大鼠相似的运动能力，但回避条件在注射氨基色素和多巴色素的大鼠中严重受损。行为影响与纹状体酪氨酸羟化酶（TH）阳性纤维丢失的程度有关。接受单侧鼻内氨基色素和多巴色素注射的大鼠黑质纹状体TH阳性纤维密度降低了47.9 +/- 5.1％和39.7 +/- 4.4％。总之，这项研究提供了证据证明将DA和L-DOPA氧化为细胞毒性醌，氨基色素和多巴色素似乎是体内氧化损伤的重要介质。

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