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使用大鼠模型研究帕金森病患者前额叶皮层的功能变化。

Functional changes in the frontal cortex in Parkinson's disease using a rat model.

机构信息

Department of Medical Imaging, Provincial Hospital Affiliated to Shandong University, Jinan, China.

出版信息

J Clin Neurosci. 2010 May;17(5):628-33. doi: 10.1016/j.jocn.2009.07.101. Epub 2010 Jan 29.

Abstract

In recent years, investigations of the pathologic mechanism of Parkinson's disease (PD) have mainly concentrated on the basal ganglia. However, recent studies have confirmed that pathological changes in PD are accompanied by functional motor changes of the cerebral cortex. Rats were injected with 6-hydroxydopamine and ascorbic acid in the right substantia nigra. In this rat model of PD, magnetic resonance spectroscopy showed the ratio of N-acetyl-aspartic acid to creatine in a lesion in the right frontal cortex was significantly lower than the same ratio in a control group of rats. The ratio of choline to creatine in a lesion in the right frontal cortex was not significantly different between the PD-model rats and control rats. In addition, the optical densities of neurofilament protein and synaptophysin positive sites decreased significantly on the side of the brain with the injury compared with the side without the injury, and with both sides in the control rats. The density of synapses in the frontal cortex on the lesioned side was decreased compared with the unlesioned side. There were abnormal changes in the presynaptic membrane, postsynaptic membrane and synaptic vesicles, and the typical synaptic structure was no longer apparent on the lesioned side. We hypothesized loss of neurons and synapses, abnormal synaptic structure and neuron and synaptic dysfunction of the frontal cortex with a lesion in the injury side of the frontal cortex in PD-model rats. These changes might have an important role in the pathologic mechanism of PD.

摘要

近年来,帕金森病(PD)病理机制的研究主要集中在基底神经节。然而,最近的研究证实,PD 的病理变化伴随着大脑皮层的功能运动变化。研究人员向右侧黑质注射了 6-羟多巴胺和抗坏血酸。在该 PD 大鼠模型中,磁共振波谱显示右侧额叶病变部位的 N-乙酰天冬氨酸与肌酸的比值明显低于对照组大鼠的相同比值。右侧额叶病变部位的胆碱与肌酸的比值在 PD 模型大鼠与对照组大鼠之间无明显差异。此外,与无损伤侧相比,损伤侧大脑的神经丝蛋白和突触小体阳性部位的光密度显著降低,而对照组大鼠两侧均如此。与未损伤侧相比,额叶皮质损伤侧的突触密度降低。损伤侧突触前膜、后膜和突触小泡出现异常变化,典型的突触结构不再明显。我们假设 PD 模型大鼠损伤侧额叶皮质损伤导致神经元和突触丢失、突触结构异常以及神经元和突触功能障碍。这些变化可能在 PD 的病理机制中起重要作用。

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