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近来报道人与灵长目动物接受呱替啶类物N- 甲基-4苯基-1,2,3,6四氢吡啶(MPTP)后,持续出现帕金森氏综合征,引起人们的关注。动物接受MPTP后,脑内代谢产物特别是化合物MPP~+(N-甲基-4苯基吡啶贮积,该化合物的毒性可被单胺氧化酶的抑制作用所阻断。因MPTP诱发的帕金森氏征与特发性帕金森氏病极相似,故MPTP样毒素可能是特发性帕金森氏病的病因,并设想用单胺氧化酶抑制剂来缓和特发性帕金森氏病的病程。运用自体放射照像术证实:标有H_3的MPTP(3H-MPTP)与鼠脑和正常人脑有着高度亲和力和特异的药理学结合力。尤其发现人类黑质的致密区结合的密度更高,作者将帕金森氏病人与普通神经科病人黑质内
It has been reported recently that human and primate animals have been receiving attention for their continued presence of Parkinson’s syndrome after receiving N-methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP). After animals received MPTP, brain metabolites, especially the compound MPP ~ + (N-methyl-4-phenylpyridine storage, the toxicity of this compound can be blocked by monoamine oxidase inhibition due to MPTP-induced Parkinson’s sign And very similar to idiopathic Parkinson’s disease, so MPTP-like toxins may be the cause of idiopathic Parkinson’s disease and envisaged monoamine oxidase inhibitors to ease the course of idiopathic Parkinson’s disease.Using autoradiography It was confirmed that HTP-labeled MPTP (3H-MPTP) has high affinity and specific pharmacological binding to mouse brain and normal human brain.It is especially found that the densification zone of human substantia nigra is more densely bound.Parkinson’s Patients and general neurology patients within the substantia nigra