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首页> 外文会议>Photons and neurons >Motor dysfunction in the tottering mouse is linked to cerebellar spontaneous low frequency oscillations revealed by flavoprotein autofluorescence optical imaging
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Motor dysfunction in the tottering mouse is linked to cerebellar spontaneous low frequency oscillations revealed by flavoprotein autofluorescence optical imaging

机译：黄素蛋白自发荧光光学成像显示，蹒跚小鼠的运动功能障碍与小脑自发性低频振荡有关

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Flavoprotein autofluorescence optical imaging is developing into a powerful research tool to study neural activity, particularly in vivo. In this study we used this imaging technique to investigate the neuronal mechanism underlying the episodic movement disorder that is characteristic of the tottering (tg) mouse, a model of episodic ataxia type 2. Both EA2 and the tg mouse are caused by mutations in the gene encoding Ca_v2.1 (P/Q-type) voltage-gated Ca~(2+) channels. These mutations result in a reduction in P/Q Ca~(2+) channel function. Both EA2 patients and tg mice have a characteristic phenotype consisting of transient motor attacks triggered by stress, caffeine or ethanol. The neural events underlying these episodes of dystonia are unknown. Flavoprotein autofluorescence optical imaging revealed spontaneous, transient, low frequency oscillations in the cerebellar cortex of the tg mouse. Lasting from 30-120 minutes, the oscillations originate in one area then spread to surrounding regions over 30 - 60 minutes. The oscillations are reduced by removing extracellular Ca~(2+) and blocking Ca_v 1.2/1.3 (L-type) Ca~(2+) channels. The oscillations are not affected by blocking AMPA receptors or by electrical stimulation of the parallel fiber - Purkinje cell circuit, suggesting the oscillations are generated intrinsically in the cerebellar cortex. Conversely, L-type Ca~(2+) agonists generate oscillations with similar properties. In the awake tg mouse, transcranial flavoprotein imaging revealed low frequency oscillations that are accentuated during caffeine induced attacks of dystonia. The oscillations increase during the attacks of dystonia and are coupled to oscillations in face and hindlimb EMG activity. These transient oscillations and the associated cerebellar dysfunction provide a novel mechanism by which an ion channel disorder results in episodic motor dysfunction.
机译：黄素蛋白自发荧光光学成像正发展成为研究神经活动（尤其是体内神经活动）的强大研究工具。在这项研究中，我们使用了这种成像技术来研究偶发性共济失调2型模型即ing（tg）小鼠的特征性发作性运动障碍的神经元机制。EA2和tg小鼠均由基因突变引起编码Ca_v2.1（P / Q型）电压门控Ca〜（2+）通道。这些突变导致P / Q Ca〜（2+）通道功能降低。 EA2患者和tg小鼠均具有特征性表型，由压力，咖啡因或乙醇触发的短暂性运动发作构成。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tg小鼠小脑皮层的自发，短暂，低频振荡。持续30-120分钟，振荡从一个区域开始，然后在30-60分钟内扩散到周围区域。通过去除细胞外Ca〜（2+）并阻断Ca_v 1.2 / 1.3（L型）Ca〜（2+）通道，可以减少振荡。振荡不受AMPA受体阻滞或平行纤维-Purkinje细胞电路的电刺激的影响，表明该振荡固有地在小脑皮质中产生。相反，L型Ca〜（2+）激动剂产生具有相似性质的振荡。在清醒的tg小鼠中，经颅黄素成像显示咖啡因引起的肌张力障碍发作时低频振荡加剧。振动在肌张力障碍发作期间增加，并与面部和后肢EMG活动的振动相关。这些短暂的振荡和相关的小脑功能障碍提供了一种新颖的机制，通过该机制离子通道失调会导致发作性运动功能障碍。

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