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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 >Effects of denervation and hyperinnervation on dopamine and serotonin systems in the rat neostriatum: implications for human Parkinson's disease.
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Effects of denervation and hyperinnervation on dopamine and serotonin systems in the rat neostriatum: implications for human Parkinson's disease.

机译：去神经支配和过度神经支配对大鼠新纹状体中多巴胺和5-羟色胺系统的影响：对人类帕金森氏病的影响。

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The research on central synaptic neurotransmission has greatly benefited from the use of the neurotoxin 2,4,5-trihydroxyphenylethylamine, or 6-hydroxydopamine (6-OHDA), that destroys catecholamine-containing neuronal cell bodies and nerve terminals. Refinements in the use of this neurotoxin led to the use of dopamine-denervated animals as models of human Parkinson's disease, in which the loss of dopaminergic neurons is a prominent feature. Here we review structural, pharmacological, and biochemical studies carried out in the adult and neonatal 6-OHDA lesioned animals. These models have become useful and interesting paradigms to examine alterations in the expression of receptors and in their sensitivity to agonist drugs; some of these modifications may underlie the altered responsiveness of the dopamine-lesioned animals to dopamine, but also to other compounds, including serotoninergic drugs. We have also reviewed studies of amino acids as well as of monoamine metabolism and of uptake mechanisms that may underlie some of the behavioural alterations in these models that have become relevant for our understanding of the sprouting and plastic properties of spared neurons, and of the alternate neuronal projections that replace lesioned terminals, enabling compensatory adaptations. Although 6-OHDA-lesioned animals, that display some biochemical characteristics of Parkinson's disease in humans, do not express all of the neurological features exhibited by patients, the increasing knowledge that can be obtained from studies in simplified experimental models will undoubtedly lead to the development of innovative drugs and other replacement therapies for degenerative brain diseases.
机译：中枢突触神经传递的研究极大地受益于使用神经毒素2,4,5-三羟基苯乙胺或6-羟基多巴胺（6-OHDA），它破坏了含有儿茶酚胺的神经元细胞体和神经末梢。对这种神经毒素的使用的改进导致使用多巴胺去神经的动物作为人类帕金森氏病的模型，其中多巴胺能神经元的丧失是突出的特征。在这里，我们回顾了在成年和新生儿6-OHDA病变动物中进行的结构，药理和生化研究。这些模型已经成为检验受体表达及其对激动剂敏感性的变化的有用和有趣的范例。这些修饰中的某些可能是多巴胺损伤动物对多巴胺的反应性改变的基础，但也可能是对其他化合物（包括5-羟色胺能药物）的反应性改变。我们还审查了氨基酸以及单胺代谢和摄取机制的研究，这些研究可能是这些模型中某些行为改变的基础，这些改变已与我们对备用神经元以及其他神经元的发芽和可塑性特性的理解相关取代病变末端的神经元投射，实现补偿性适应。尽管6-OHDA损伤的动物虽然表现出人类帕金森氏病的某些生化特征，但不能表达患者表现出的所有神经系统特征，但通过简化的实验模型进行研究所获得的不断增长的知识无疑将导致其发展。用于退行性脑疾病的创新药物和其他替代疗法的开发。

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