• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The European Journal of Neuroscience >Dopamine receptor supersensitivity in rat subthalamus after 6-hydroxydopamine lesions.
【24h】

Dopamine receptor supersensitivity in rat subthalamus after 6-hydroxydopamine lesions.

机译：6-羟基多巴胺损伤后大鼠丘脑下的多巴胺受体超敏反应。

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

The subthalamic nucleus (STN) receives direct dopaminergic innervation from the substantia nigra pars compacta, but the importance of this input in the pathophysiology of parkinsonism remains to be determined. We used whole-cell patch-clamp recordings in brain slices to study presynaptic dopaminergic modulation of synaptic inputs to the STN in unilateral 6-hydroxydopamine (6-OHDA)-lesioned rats. Here, we report that dopamine was more potent for inhibiting GABA IPSCs and glutamate EPSCs in the STN ipsilateral to the lesion, and was less potent for suppressing IPSCs and EPSCs in the STN contralateral to the lesion, compared with the effects of dopamine in control STN. Dopamine reduced IPSCs with an IC50 value of 20.9 +/- 3.6 micro m in control STN, whereas IC50 values were 0.83 +/- 0.15 and 55.1 +/- 11.1 micro m in STN ipsilateral and contralateral to 6-OHDA lesions, respectively. Dopamine also inhibited EPSCs with an IC50 value of 12.8 +/- 2.8 micro m in control STN, whereas IC50 values were 4.5 +/- 0.9and 41.6 +/- 9.8 micro m in STN ipsilateral and contralateral to 6-OHDA lesions, respectively. Results with paired stimuli to evoke EPSCs and IPSCs suggest that endogenous dopamine acts presynaptically to inhibit transmitter release in the STN. These results show that chronic dopamine denervation significantly alters the regulation of synaptic input to the STN. Our results also suggest that the STN may be an important target for levodopa therapy in Parkinson's disease.
机译：丘脑下核（STN）从黑质致密部直接接受多巴胺能神经支配，但这种输入在帕金森氏病病理生理学中的重要性尚待确定。我们在脑切片中使用全细胞膜片钳记录来研究单侧6-羟基多巴胺（6-OHDA）损伤大鼠的突触输入到STN的突触前多巴胺能调节。在这里，我们报道多巴胺对病变STN同侧的GABA IPSC和谷氨酸EPSC的抑制作用更强，而对侧病变STN对IPSC和EPSC的抑制作用较之对照STN多巴胺更弱。多巴胺可降低IPSC，对照STN的IC50值为20.9 +/- 3.6微米，而STN同侧和对侧6-OHDA病变的IC50值分别为0.83 +/- 0.15和55.1 +/- 11.1微米。多巴胺还抑制EPSC，对照STN的IC50值为12.8 +/- 2.8微米，而STN同侧和对侧6-OHDA病变的IC50值分别为4.5 +/- 0.9和41.6 +/- 9.8微米。与激发EPSC和IPSC的成对刺激的结果表明，内源性多巴胺可先突触地抑制STN中的递质释放。这些结果表明，慢性多巴胺去神经支配显着改变了STN突触输入的调节。我们的结果还表明，STN可能是帕金森氏病左旋多巴治疗的重要靶标。

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