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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 >Chronic D1 and D2 dopaminomimetic treatment of MPTP-denervated monkeys: effects on basal ganglia GABA(A)/benzodiazepine receptor complex and GABA content.
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Chronic D1 and D2 dopaminomimetic treatment of MPTP-denervated monkeys: effects on basal ganglia GABA(A)/benzodiazepine receptor complex and GABA content.

机译：MPTP去神经猴的慢性D1和D2多巴胺模拟治疗：对基底神经节GABA（A）/苯并二氮杂receptor受体复合物和GABA含量的影响。

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The effect of various chronic dopaminergic treatments in 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) monkeys on the brain gamma-aminobutyric acid type A (GABA(A)) /benzodiazepine receptor complex and GABA content was investigated in order to assess the GABAergic involvement in dopaminomimetic-induced dyskinesia. Three MPTP monkeys received for one month pulsatile administrations of the D1 dopamine (DA) receptor agonist SKF 82958 whereas three others received the same dose of SKF 82958 by continuous infusion. A long acting D2 DA receptor agonist, cabergoline, was given to another three animals. Untreated MPTP as well as naive control animals were also included. Pulsatile SKF 82958 relieved parkinsonian symptoms but was also associated with dyskinesia in two of the three animals whereas animals treated continuously with SKF 82958 remained as untreated MPTP monkeys. Chronic cabergoline administration improved motor response with no persistent dyskinesia. MPTP treatment induced a decrease of 3H-flunitrazepam binding in the medial anterior part of caudate-putamen and an increase in the internal segment of globus pallidus (GPi) which was in general unchanged by pulsatile or continuous SKF 82958 administration. Throughout the striatum, binding of 3H-flunitrazepam remained reduced in MPTP monkeys treated with cabergoline but was not significantly lower than untreated MPTP monkeys. Moreover, cabergoline treatment reversed the MPTP-induced increase in 3H-flunitrazepam binding in the GPi. GABA concentrations remained unchanged in the striatum, external segment of globus pallidus and GPi following MPTP denervation. Pulsatile but not continuous SKF 82958 administration decreased putamen GABA content whereas cabergoline treatment decreased caudate GABA. No alteration in GABA levels were observed in the GPe and GPi following the experimental treatments. These results suggest that: (1) D2-like receptor stimulation with cabergoline modulates GABA(A) receptor density in striatal subregions anatomically related to associative cortical afferent and (2) the absence of dyskinesia in dopaminomimetic-treated monkeys might be associated with the reversal of the MPTP-induced upregulation of the GABA(A)/benzodiazepine receptor complex in the Gpi.
机译：1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）猴子中各种慢性多巴胺能治疗对脑A型γ-氨基丁酸（GABA（A））/苯并二氮杂receptor受体复合物和GABA的影响为了评估GABA能参与多巴胺模拟物引起的运动障碍，研究了其含量。三只MPTP猴子接受D1多巴胺（DA）受体激动剂SKF 82958的脉动给药一个月，而其他三只猴子则通过连续输注接受相同剂量的SKF 82958。将长效D2 DA受体激动剂卡麦角林用于另外三只动物。还包括未治疗的MPTP以及幼稚的对照动物。搏动性SKF 82958缓解了帕金森病症状，但在三只动物中的两只也与运动障碍有关，而连续用SKF 82958治疗的动物仍为未经治疗的MPTP猴子。长期使用卡麦角林改善了运动反应，没有持续的运动障碍。 MPTP处理可导致尾状-丘脑内侧前部3H-氟硝西binding结合减少，而苍白球（GPi）的内部部分增加，这通常可通过脉冲或连续SKF 82958给药而保持不变。在整个纹状体中，卡麦角林治疗的MPTP猴子中3H-氟硝西m的结合仍然减少，但没有显着低于未治疗的MPTP猴子。此外，卡麦角林治疗逆转了MPTP诱导的GPi中3H-氟硝西m结合的增加。 MPTP去神经后，纹状体，苍白球外段和GPi中的GABA浓度保持不变。脉冲但不连续的SKF 82958给药可降低壳聚糖GABA含量，而卡麦角林治疗可降低尾状GABA。实验处理后，在GPe和GPi中未观察到GABA水平的改变。这些结果表明：（1）卡麦角林刺激D2样受体可调节与联想皮层传入相关的纹状体亚区GABA（A）受体密度，（2）经多巴胺模拟物治疗的猴子不存在运动障碍可能与逆转有关MPTP诱导的Gpi中GABA（A）/苯并二氮杂receptor受体复合物的上调。

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