Ghorayeb I, Fernagut P O, Stefanova N, Wenning G K, Bioulac B, Tison F
CNRS-UMR 5543, Université Victor Segalen Bordeaux 2, 146, rue Léo-Saignat, 33076 Bordeaux Cedex, France.
Neurosci Lett. 2002 Dec 19;335(1):34-8. doi: 10.1016/s0304-3940(02)01137-0.
We conducted a new chronic sequential 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 3-nitropropionic acid (3NP) intoxication paradigm in two female monkeys in order to reproduce the striatonigral degeneration type of levodopa-unresponsive parkinsonism. A comparison was made with MPTP-, 3NP-intoxicated and control monkeys. A levodopa-responsive parkinsonism emerged in all MPTP-treated monkeys. During subsequent 3NP intoxication, one of the two MPTP +3NP monkeys exhibited hindlimb dystonia concomitantly with a reduced levodopa response. All MPTP-monkeys had severe cell loss in the substantia nigra pars compacta (>70%), but 3NP-induced discrete lesioned areas and cell loss predominantly in the putamen appeared only in the dystonic and levodopa-unresponsive animal. We propose that the appearance of dystonia after 3NP intoxication following dopaminergic striatal denervation is the key symptom predictive of the loss of dopaminergic response.
为了重现左旋多巴无反应型帕金森病的纹状体黑质变性类型,我们对两只雌性猴子进行了一种新的慢性序贯1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)和3-硝基丙酸(3NP)中毒模型。并与MPTP、3NP中毒的猴子及对照猴子进行了比较。所有接受MPTP治疗的猴子都出现了左旋多巴反应性帕金森病。在随后的3NP中毒期间,两只MPTP + 3NP猴子中的一只出现了后肢肌张力障碍,同时左旋多巴反应降低。所有MPTP猴子的黑质致密部都有严重的细胞丢失(>70%),但3NP诱导的离散病变区域和主要在壳核的细胞丢失仅出现在肌张力障碍和左旋多巴无反应的动物中。我们认为,多巴胺能纹状体去神经支配后3NP中毒时肌张力障碍的出现是多巴胺能反应丧失的关键预测症状。