• 主题
高级搜索  >
历史搜索 清空历史
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 >Neurochemical changes in the striatum of dyskinetic rats after administration of the cannabinoid agonist WIN55,212-2.
【24h】

Neurochemical changes in the striatum of dyskinetic rats after administration of the cannabinoid agonist WIN55,212-2.

机译：给予大麻素激动剂WIN55,212-2后，运动障碍大鼠纹状体中的神经化学变化。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Chronic use of levodopa, the most effective treatment for Parkinson's disease, causes abnormal involuntary movements named dyskinesias, which are linked to maladaptive changes in plasticity and disturbances of dopamine and glutamate neurotransmission in the basal ganglia. Dyskinesias can be modeled in rats with unilateral 6-hydroxydopamine lesions by repeated administration of low doses of levodopa (6 mg/kg, s.c.). Previous studies from our lab showed that sub-chronic treatment with the cannabinoid agonist WIN55,212-2 attenuates levodopa-induced dyskinesias at doses that do not interfere with physiological motor function. To investigate the neurochemical changes underlying WIN55,212-2 anti-dyskinetic effects, we used in vivo microdialysis to monitor extracellular dopamine and glutamate in the dorsal striatum of both the hemispheres of freely moving 6-hydroxydopamine-treated, SHAM-operated and intact rats receiving levodopa acutely or chronically (11 days), and studied how sub-chronic WIN55,212-2 (1 injection x 3 days, 20 min before levodopa) affected these neurochemical outputs. Our data indicate that: (1) the 6-hydroxydopamine lesion decreases dopamine turnover in the denervated striatum; (2) levodopa injection reduces extracellular glutamate in the side ipsilateral to the lesion of dyskinetic rats; (3) sub-chronic WIN55,212-2 prevents levodopa-induced glutamate volume transmission unbalances across the two hemispheres; and (4) levodopa-induced dyskinesias are inversely correlated with glutamate levels in the denervated striatum. These data indicate that the anti-dyskinetic properties of WIN55,212-2 are accompanied by changes of dopamine and glutamate outputs in the two brain hemispheres of 6-hydroxydopamine-treated rats.
机译：长期使用左旋多巴是治疗帕金森氏病的最有效方法，会引起异常的不自主运动，称为运动障碍，这与可塑性的不良适应性变化以及基底神经节中多巴胺和谷氨酸神经传递的紊乱有关。可以通过反复给予低剂量的左旋多巴（6 mg / kg，s.c.）在单侧6-羟基多巴胺损伤的大鼠中模拟运动障碍。我们实验室先前的研究表明，使用大麻素激动剂WIN55,212-2进行亚慢性治疗可缓解左旋多巴诱发的运动障碍，且剂量不会干扰生理运动功能。为了研究WIN55,212-2抗运动障碍作用背后的神经化学变化，我们使用了体内微透析法来监测自由移动的6-羟基多巴胺处理，SHAM手术和完整大鼠的两个半球背侧纹状体的细胞外多巴胺和谷氨酸。急性或慢性（11天）接受左旋多巴，并研究亚慢性WIN55,212-2（1次注射x 3天，左旋多巴前20分钟）如何影响这些神经化学输出。我们的数据表明：（1）6-羟基多巴胺损伤减少了失神经纹状体中多巴胺的转化; （2）左旋多巴注射液可减少运动障碍大鼠病灶同侧的细胞外谷氨酸。 （3）亚慢性WIN55,212-2可防止左旋多巴引起的谷氨酸在两个半球之间的体积传输不平衡; （4）左旋多巴诱发的运动障碍与失神经纹状体中的谷氨酸水平呈负相关。这些数据表明，在用6-羟基多巴胺治疗的大鼠的两个脑半球中，WIN55,212-2的抗运动特性伴随着多巴胺和谷氨酸输出的变化。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号