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首页> 外文期刊>Journal of Neurophysiology >Low-frequency oscillations in the cerebellar cortex of the tottering mouse.
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Low-frequency oscillations in the cerebellar cortex of the tottering mouse.

机译：蹒跚小鼠的小脑皮质中的低频振荡。

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The tottering mouse is an autosomal recessive disorder involving a missense mutation in the gene encoding P/Q-type voltage-gated Ca(2+) channels. The tottering mouse has a characteristic phenotype consisting of transient attacks of dystonia triggered by stress, caffeine, or ethanol. The neural events underlying these episodes of dystonia are unknown. Flavoprotein autofluorescence optical imaging revealed transient, low-frequency oscillations in the cerebellar cortex of anesthetized and awake tottering mice but not in wild-type mice. Analysis of the frequencies, spatial extent, and power were used to characterize the oscillations. In anesthetized mice, the dominant frequencies of the oscillations are between 0.039 and 0.078 Hz. The spontaneous oscillations in the tottering mouse organize into high power domains that propagate to neighboring cerebellar cortical regions. In the tottering mouse, the spontaneous firing of 83% (73/88) of cerebellar cortical neurons exhibit oscillations at the same low frequencies. The oscillations are reduced by removing extracellular Ca(2+) and blocking L-type Ca(2+) channels. The oscillations are likely generated intrinsically in the cerebellar cortex because they are not affected by blocking AMPA receptors or by electrical stimulation of the parallel fiber-Purkinje cell circuit. Furthermore, local application of an L-type Ca(2+) agonist in the tottering mouse generates oscillations with similar properties. The beam-like response evoked by parallel fiber stimulation is reduced in the tottering mouse. In the awake tottering mouse, transcranial flavoprotein imaging revealed low-frequency oscillations that are accentuated during caffeine-induced attacks of dystonia. During dystonia, oscillations are also present in the face and hindlimb electromyographic (EMG) activity that become significantly coherent with the oscillations in the cerebellar cortex. These low-frequency oscillations and associated cerebellar cortical dysfunction demonstrate a novel abnormality in the tottering mouse. These oscillations are hypothesized to be involved in the episodic movement disorder in this mouse model of episodic ataxia type 2.
机译：摇摇欲坠的小鼠是常染色体隐性遗传疾病，涉及编码P / Q型电压门控Ca（2+）通道的基因中的错义突变。蹒跚的老鼠具有特征性的表型，包括由压力，咖啡因或乙醇引发的肌张力障碍的短暂发作。这些肌张力障碍发作的神经事件尚不清楚。黄素蛋白自发荧光光学成像显示麻醉和清醒的小脑小鼠的小脑皮层出现短暂的低频振荡，而野生型小鼠则没有。频率，空间范围和功率的分析被用来表征振荡。在麻醉的小鼠中，振荡的主要频率在0.039和0.078 Hz之间。蹒跚小鼠的自发振荡组织成高功率域，并传播到邻近的小脑皮质区域。在摇摇欲坠的小鼠中，小脑皮质神经元的自发放电有83％（73/88）在相同的低频下表现出振荡。通过删除细胞外Ca（2+）和阻止L型Ca（2+）通道来减少振荡。振荡很可能会在小脑皮层内固有地产生，因为它们不受AMPA受体阻滞或平行纤维-浦肯野细胞电路的电刺激的影响。此外，在蹒跚学步的小鼠中L型Ca（2+）激动剂的本地应用会产生具有类似属性的振荡。蹒跚小鼠中平行纤维刺激引起的束状反应减少。在清醒的老鼠体内，经颅黄素蛋白成像显示低频振荡在咖啡因诱发的肌张力障碍发作中加剧。在肌张力障碍期间，面部和后肢肌电图（EMG）活动中也出现振动，这些活动与小脑皮层中的振动变得非常连贯。这些低频振荡和相关的小脑皮质功能紊乱表明，在蹒跚学步的小鼠中出现了新的异常。假定这些振荡与这种情节性共济失调2型小鼠模型的情节性运动障碍有关。

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