Kucheryanu V G, Kryzhanovskii G N
Laboratory of General Pathophysiology of Nervous System, Institute of General Pathology and Pathological Physiology, Russian Academy of Medical Sciences, Moscow.
Bull Exp Biol Med. 2000 Jul;130(7):629-32. doi: 10.1007/BF02682089.
Intranigral administration of glutamate to rats with parkinsonian syndrome induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine augmented the development of parkinsonian symptoms (oligokinesia and muscular rigidity), but did not affect motor activity of intact animals. Memantine administered intraperitoneally in parallel with induction of parkinsonian syndrome weakened the development of oligokinesia and muscular rigidity in a dose-dependent manner starting from 5 mg/kg and abolished toxic effect of glutamate. Ketamine (15 mg/kg) under the same conditions less potently prevented the development of oligokinesia, did not prevent the development of muscular rigidity, and did not antagonize glutamate toxicity. The data attest to an important role of glutamate and activation of N-methyl-D-aspartate receptors in the induction and development of parkinsonian syndrome.
向由1-甲基-4-苯基-1,2,3,6-四氢吡啶诱导的帕金森综合征大鼠脑黑质内注射谷氨酸，会加剧帕金森症状（运动减少和肌肉强直）的发展，但不影响正常动物的运动活性。在诱导帕金森综合征的同时腹腔注射美金刚，从5mg/kg开始以剂量依赖方式减弱运动减少和肌肉强直的发展，并消除谷氨酸的毒性作用。在相同条件下，氯胺酮（15mg/kg）预防运动减少发展的效力较弱，不能预防肌肉强直的发展，也不能拮抗谷氨酸毒性。这些数据证明谷氨酸和N-甲基-D-天冬氨酸受体的激活在帕金森综合征的诱导和发展中起重要作用。
