Activity-Dependent Plasticity of Spike Pauses in Cerebellar Purkinje Cells.
Activity-Dependent Plasticity of Spike Pauses in Cerebellar Purkinje Cells.
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DOI：
10.1016/j.celrep.2016.02.054
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发表时间：
2016-03-22
期刊：
影响因子：
8.8
通讯作者：
Hansel C
中科院分区：
文献类型：
--
作者：
Grasselli G;He Q;Wan V;Adelman JP;Ohtsuki G;Hansel C
在几种类型的神经元中已经描述了内在兴奋性的可塑性，但是在脑可塑性和学习中的非突触机制的重要性仍然是难以捉摸的。小脑浦肯野细胞是抑制性神经元，其自发地以高频率激发动作电位，并通过在突触激活时产生特征性的尖峰爆发-暂停序列来调节小脑核中的靶细胞中的活性。使用膜片钳记录从小鼠浦肯野细胞，我们发现，去极化触发的内在可塑性增强锋电位发射和缩短的时间的锋电位暂停。缺乏SK 2型钾通道的小鼠（SK 2 −/−小鼠）和使用SK通道阻断剂apamin的闭塞实验中不存在突触可塑性，而apamin洗入模拟暂停减少。我们的研究结果表明，尖峰暂停可以通过活动依赖性，完全非突触，SK2通道依赖性机制进行调节，并建议暂停可塑性-通过改变浦肯野细胞的输出-可能是至关重要的小脑信息存储和学习。
Plasticity of intrinsic excitability has been described in several types of neurons, but the significance of non-synaptic mechanisms in brain plasticity and learning remains elusive. Cerebellar Purkinje cells are inhibitory neurons that spontaneously fire action potentials at high frequencies and regulate activity in their target cells in the cerebellar nuclei by generating a characteristic spike burst–pause sequence upon synaptic activation. Using patch-clamp recordings from mouse Purkinje cells, we find that depolarization-triggered intrinsic plasticity enhances spike firing and shortens the duration of spike pauses. Pause plasticity is absent from mice lacking SK2-type potassium channels (SK2−/− mice) and in occlusion experiments using the SK channel blocker apamin, while apamin wash-in mimics pause reduction. Our findings demonstrate that spike pauses can be regulated through an activity-dependent, exclusively non-synaptic, SK2 channel-dependent mechanism and suggest that pause plasticity—by altering the Purkinje cell output—may be crucial to cerebellar information storage and learning.