Theoretical Neurobiology, University of Antwerp Antwerpen, Belgium.
Front Cell Neurosci. 2013 Nov 13;7:205. doi: 10.3389/fncel.2013.00205. eCollection 2013.
The complex spike (CS) in cerebellar Purkinje Cells (PC) is not an all-or-nothing phenomena as originally proposed, but shows variability depending on the spiking behavior of the Inferior Olive and intrinsic variability in the number and shape of spikelets. The potassium channel Kv3.3b, which has been proposed to undergo developmental changes during the postnatal PC maturation, has been shown to be crucial for the repolarization of the spikelets in the CS. We address here the regulation of the intrinsic CS variability by the expression of inactivating Kv3.3 channels in PCs by combining patch-clamp recordings and single-cell PCR methods on the same neurons, using a technique that we recently optimized to correlate single cell transcription levels with membrane ion channel electrophysiology. We show that while the inactivating TEA sensitive Kv3.3 current peak intensity increases with postnatal age, the channel density does not, arguing against postnatal developmental changes of Kv3.3b expression. Real time PCR of Kv3.3b showed a high variability from cell to cell, correlated with the Kv3.3 current density, and suggesting that there are no mechanisms regulating these currents beyond the mRNA pool. We show a significant correlation between normalized quantity of Kv3.3b mRNA and both the number of CS spikelets and their rate of voltage fluctuation, linking the intrinsic CS shape directly to the Kv3.3b mRNA pool. Comparing the observed cell-to-cell variance with studies on transcriptional noise suggests that fluctuations of the Kv3.3b mRNA pool are possibly not regulated but represent merely transcriptional noise, resulting in intrinsic variability of the CS.
小脑浦肯野细胞(PC)中的复杂峰(CS)并非最初提出的全有或全无现象,而是根据下橄榄核的放电行为和峰簇数量和形状的固有变异性而变化。钾通道 Kv3.3b 被认为在 PC 出生后成熟过程中发生发育变化,对于 CS 中峰簇的复极化至关重要。我们在这里通过在相同神经元上结合膜片钳记录和单细胞 PCR 方法,利用我们最近优化的技术来将单细胞转录水平与膜离子通道电生理学相关联,来解决 PC 中失活 Kv3.3 通道表达对固有 CS 变异性的调节问题。我们发现,虽然失活的 TEA 敏感 Kv3.3 电流峰值强度随出生后年龄的增加而增加,但通道密度没有增加,这表明 Kv3.3b 的表达没有出生后发育变化。实时 PCR 显示 Kv3.3b 的细胞间变异性很高,与 Kv3.3 电流密度相关,表明除了 mRNA 池之外,没有其他机制可以调节这些电流。我们发现 Kv3.3b mRNA 的归一化量与 CS 峰簇的数量及其电压波动率之间存在显著相关性,直接将 CS 的固有形状与 Kv3.3b mRNA 池联系起来。将观察到的细胞间方差与转录噪声研究进行比较表明,Kv3.3b mRNA 池的波动可能不受调节,而仅仅是转录噪声,导致 CS 的固有变异性。