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帕金森病的病理同步有什么危害?

What Harm Does Pathological Synchronization in Parkinson's Disease Do?
课程网址: http://videolectures.net/mitworld_brown_whdpspdd/  
主讲教师: Peter Brown
开课单位: 伦敦大学学院
开课时间: 2010-08-09
课程语种: 英语
中文简介:
就像在收音机FM频段的电台中进行调谐一样,神经科学家可以检测出我们大脑的特定频率。就像在收音机上一样,预计会有一点噪音和静电。在帕金森病(PD)中,正如彼得布朗及其同事所发现的那样,过多的某种频率是一件坏事。基底神经节中的神经元产生一种过度同步的β频率(在20Hz范围内),这似乎与帕金森病的一些症状有关。布朗森的讲话概述了在PD中记录这种“振荡同步”的努力,以弄清楚它背后的生理机制,并将β同步直接与PD患者的关键症状联系起来,如僵硬和运动迟缓(执行动作缓慢)。科学家可以检测丘脑底核(基底神经节的一个关键组成部分)中的神经元簇,以20赫兹“跳动”。布朗说,这些神经元的“夸张同步”似乎与神经递质多巴胺的慢性丧失有关。普通受试者有“相当数量的健康β活动,”布朗指出,当这些受试者进行自愿运动时,例如伸出食指,β活动受到抑制。布朗说,在PD患者中,不受控制的β活动似乎会“以牺牲自愿运动为代价来促进姿势收缩。”布朗和其他人已经记录了接受两种关键治疗方法的PD患者大脑的活动:深部脑刺激(植入电极的地方)大脑试图打破正常神经元放电的模式)和多巴胺能治疗。这两种方法都可以缓解缓慢移动和僵硬的症状。在这两种治疗过程中抑制了过度的β振荡。这是“相关证据”,布朗说,β活动是症状背后的原因。科学家正试图将这些点连接起来,并找到一个因果关系:在刺激丘脑底核的神经元以20Hz击败后,他们观察到运动减慢了20%。布朗正在进行另外的研究,这些研究提供了循环脑通路PD的证据,不仅涉及基底神经节,而且涉及皮质的部分,其具有“20Hz活动的先天倾向”,引起运动迟缓和僵硬,并且可以是受到多巴胺输入的阻碍。最后,布朗承认他必须将“测试版故事......降到现实”,因为它似乎与其他PD症状(例如震颤)无关,并且“我在这里一直是测试沙文主义者,并且忽略了其他频率。 ”
课程简介: Like tuning in a station on the FM band of a radio, neuroscientists can detect the particular frequencies of our brains in action. And just as on the radio, a little noise and static is to be expected. In Parkinson’s Disease (PD), as Peter Brown and colleagues are finding, too much of a certain type of frequency is a bad thing. Neurons in the basal ganglia produce a kind of overly synchronized beta frequency (in the 20 Hz range) that seems deeply implicated in some of the telltale symptoms of Parkinson’s. Brown’s talk outlines efforts to record this “oscillatory synchrony” in PD, to figure out the physiological mechanisms behind it, and to connect beta synchrony directly to such key symptoms in PD patients as rigidity and bradykinesia (slowness in executing movements). Scientists can detect clusters of neurons in the subthalamic nucleus (a key component of the basal ganglia) “beating” at 20 Hz. Brown says the “exaggerated synchrony” of these neurons seems to have something to do with a chronic loss of the neurotransmitter dopamine. Ordinary subjects have a “fair amount of healthy beta activity,” notes Brown, and when these subjects engage in voluntary movements, such as extending a forefinger, the beta activity is suppressed. But in PD patients, says Brown, uncontrolled beta activity seems to promote postural contraction “at the expense of voluntary movement.” Brown and others have recorded activity in the brains of PD patients undergoing two key treatments, Deep Brain Stimulation (where electrodes implanted in the brain try to break the pattern of normal neuronal firing), and dopaminergic therapy. Both methods relieve the symptoms of slow movement and rigidity. Excessive beta oscillations are suppressed during these two treatments. This is “correlative evidence,” says Brown, that beta activity is behind the symptoms. Scientists are trying to connect the dots, and find a causal link: After stimulating the neurons of the subthalamic nucleus to beat at 20 Hz, they observe a 20% slowing of movement. Brown is conducting additional studies that provide evidence in PD of a looping brain pathway involving not just the basal ganglia, but parts of the cortex, which has an “innate tendency for activity at 20 Hz,” causing bradykinesia and rigidity, and which can be damped by the input of dopamine. In closing, Brown acknowledges he must bring “the beta story …down to reality,” since it doesn’t seem to connect to other PD symptoms such as tremor, and “I’ve been a beta chauvinist here, and ignored other frequencies.”
关 键 词: 神经节; 神经元; 帕金森病
课程来源: 视频讲座网
最后编审: 2019-05-29:lxf
阅读次数: 60