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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Low-pass filter properties of basal ganglia cortical muscle loops in the normal and MPTP primate model of parkinsonism.
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Low-pass filter properties of basal ganglia cortical muscle loops in the normal and MPTP primate model of parkinsonism.

机译:在正常和MPTP灵长类帕金森病模型中,基底节神经皮层肌肉环的低通滤波器特性。

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Oscillatory bursting activity is commonly found in the basal ganglia (BG) and the thalamus of the parkinsonian brain. The frequency of these oscillations is often similar to or higher than that of the parkinsonian tremor, but their relationship to the tremor and other parkinsonian symptoms is still under debate. We studied the frequency dependency of information transmission in the cortex-BG and cortex-periphery loops by recording simultaneously from multiple electrodes located in the arm-related primary motor cortex (MI) and in the globus pallidus (GP) of two vervet monkeys before and after 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment and induction of parkinsonian symptoms. We mimicked the parkinsonian bursting oscillations by stimulating with 35 ms bursts given at different frequencies through microelectrodes located in MI or GP while recording the evoked neuronal and motor responses. In the normal state, microstimulation of MI or GP does not modulate the discharge rate in the other structure. However, the functional-connectivity between MI and GP is greatly enhanced after MPTP treatment. In the frequency domain, GP neurons usually responded equally to 1-15 Hz stimulation bursts in both states. In contrast, MI neurons demonstrated low-pass filter properties, with a cutoff frequency above 5 Hz for the MI stimulations, and below 5 Hz for the GP stimulations. Finally, muscle activation evoked by MI microstimulation was markedly attenuated at frequencies higher than 5 Hz. The low-pass properties of the pathways connecting GP to MI to muscles suggest that parkinsonian tremor is not directly driven by the BG 5-10 Hz burst oscillations despite their similar frequencies.
机译:震荡爆发活动通常在基底神经节(BG)和帕金森氏脑的丘脑中发现。这些振荡的频率通常类似于或高于帕金森氏震颤的频率,但是它们与震颤和其他帕金森氏症状的关系仍在争论中。我们通过同时记录位于手臂相关的主运动皮层(MI)和两个黑长尾猴的苍白球(GP)中的多个电极,来同时记录皮质BG和皮质外围回路中信息传输的频率依赖性。 1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)治疗和诱发帕金森病症状后。我们通过记录MI和GP中的微电极,同时记录不同的神经元和运动反应,通过以不同频率给予35 ms的脉冲刺激来模拟帕金森氏脉冲爆发振荡。在正常状态下,MI或GP的微刺激不会调节其他结构的放电速率。但是,MPTP处理后,MI和GP之间的功能连接性大大增强。在频域中,GP神经元通常在两种状态下均对1-15 Hz的刺激猝发做出同样的反应。相反,MI神经元表现出低通滤波器特性,对于MI刺激,截止频率高于5 Hz,对于GP刺激,截止频率低于5 Hz。最后,MI微刺激引起的肌肉激活在高于5 Hz的频率下明显减弱。 GP和MI连接至肌肉的路径的低通特性表明,尽管频率相似,但帕金森氏震颤并非直接由BG 5-10 Hz爆发振荡驱动。

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