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L 型 Cav1.2 钙通道参与了 6-羟多巴胺诱导的大鼠神经毒性。

L-type Cav1.2 calcium channel is involved in 6-hydroxydopamine-induced neurotoxicity in rats.

机构信息

Department of Physiology, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders and State Key Disciplines: Physiology, Medical College of Qingdao University, Qingdao 266071, China.

出版信息

Neurotox Res. 2012 Apr;21(3):266-70. doi: 10.1007/s12640-011-9271-x. Epub 2011 Sep 7.

Abstract

Evidence suggested that L-type calcium channels may play a key role in the pathogenesis of dopaminergic neuron degeneration. In the present study, effects of L-type Cav1.2 calcium channel on 6-hydroxydopamine (6-OHDA)-induced neurotoxicity were investigated. By the semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) studies, we showed that the expression of L-type Cav1.2 calcium channel α1 subunit mRNA increased in the substantia nigra (SN) of 6-OHDA-lesioned rats. Treatment with nifedipine could improve the apomorphine-induced rotation behavior in 6-OHDA-lesioned rats. Using high-performance liquid chromatography electrochemical detection, we also observed that nifedipine partly restored 6-OHDA-induced dopamine depletion in the striatum of rats. These results suggest that the L-type Cav1.2 calcium channel is associated with the development and progression of dopaminergic neuron degeneration.

摘要

有证据表明,L 型钙通道可能在多巴胺能神经元变性的发病机制中起关键作用。在本研究中,研究了 L 型 Cav1.2 钙通道对 6-羟基多巴胺(6-OHDA)诱导的神经毒性的影响。通过半定量逆转录聚合酶链反应(RT-PCR)研究,我们发现在 6-OHDA 损伤的大鼠黑质(SN)中,L 型 Cav1.2 钙通道α1 亚基 mRNA 的表达增加。硝苯地平治疗可改善 6-OHDA 损伤大鼠的阿扑吗啡诱导的旋转行为。使用高效液相色谱电化学检测,我们还观察到硝苯地平部分恢复了 6-OHDA 诱导的大鼠纹状体多巴胺耗竭。这些结果表明,L 型 Cav1.2 钙通道与多巴胺能神经元变性的发展和进展有关。

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