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肾上腺自体移植或单纯空洞形成后偏侧帕金森病猴的长期评估

Long-term evaluation of hemiparkinsonian monkeys after adrenal autografting or cavitation alone.

作者信息

Plunkett R J, Bankiewicz K S, Cummins A C, Miletich R S, Schwartz J P, Oldfield E H

机构信息

Laboratory of Central Nervous System Implantation, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland.

出版信息

J Neurosurg. 1990 Dec;73(6):918-26. doi: 10.3171/jns.1990.73.6.0918.

DOI:10.3171/jns.1990.73.6.0918
PMID:2230974
Abstract

Autografts of adrenal medulla were implanted into preformed cavities in the caudate nuclei of four rhesus monkeys with hemiparkinsonism induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Five other hemiparkinsonian monkeys underwent caudate cavitation, but received no tissue implant. All of the animals had marked bradykinesia of the affected arm and stable apomorphine-induced turning before cavitation or implantation. Moderate behavioral recovery was seen in all five monkeys with cavitation and two of the three monkey with long-term adrenal autografts (the fourth adrenal recipient was sacrificed 10 days after grafting). The improvement occurred months after the procedure and was not as early or as complete as that seen after fetal dopaminergic grafts. Surviving adrenal tissue was found only in the animal that showed no behavioral recovery. The other two adrenal autograft recipients (with no surviving adrenal medulla) and all of the animals with cavitation had ingrowth of dopaminergic fibers from the area olfactoria and nucleus accumbens into the caudate, oriented toward the cavity. These findings show that the mechanism of improvement after adrenal medullary implants for parkinsonism is not dopamine secretion by chromaffin cells, but may be related to the sprouted host fibers. The results also indicate that the limited recovery after adrenal implants in parkinsonian patients may be a result of the cavitation, and not necessarily the result of tissue implantation.

摘要

将肾上腺髓质自体移植片植入4只患1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)诱导的偏侧帕金森病的恒河猴尾状核内预先形成的腔隙中。另外5只偏侧帕金森病猴接受了尾状核造腔,但未接受组织移植。所有动物在造腔或移植前患侧手臂均有明显的运动迟缓,且阿扑吗啡诱导的旋转行为稳定。在所有5只接受造腔的猴子以及3只接受长期肾上腺自体移植的猴子中的2只(第4只肾上腺移植接受者在移植后10天被处死)出现了中度行为恢复。改善在手术后数月出现,不如胎儿多巴胺能移植后出现得早或彻底。仅在未出现行为恢复的动物中发现了存活的肾上腺组织。另外2只肾上腺自体移植接受者(无存活的肾上腺髓质)以及所有接受造腔的动物,均有来自嗅区和伏隔核的多巴胺能纤维长入尾状核,朝向腔隙。这些发现表明,帕金森病肾上腺髓质植入后改善的机制不是嗜铬细胞分泌多巴胺,而可能与宿主纤维的芽生有关。结果还表明,帕金森病患者肾上腺植入后恢复有限可能是造腔的结果,而不一定是组织移植的结果。

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