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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Spike-time precision and network synchrony are controlled by the homeostatic regulation of the D-type potassium current.
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Spike-time precision and network synchrony are controlled by the homeostatic regulation of the D-type potassium current.

机译：Spike-Time Precision和网络同步由D型钾电流的稳态调节控制。

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摘要

Homeostatic plasticity of neuronal intrinsic excitability (HPIE) operates to maintain networks within physiological bounds in response to chronic changes in activity. Classically, this form of plasticity adjusts the output firing level of the neuron through the regulation of voltage-gated ion channels. Ion channels also determine spike timing in individual neurons by shaping subthreshold synaptic and intrinsic potentials. Thus, an intriguing hypothesis is that HPIE can also regulate network synchronization. We show here that the dendrotoxin-sensitive D-type K+ current (ID) disrupts the precision of AP generation in CA3 pyramidal neurons and may, in turn, limit network synchronization. The reduced precision is mediated by the sequence of outward ID followed by inward Na+ current. The homeostatic downregulation of ID increases both spike-time precision and the propensity for synchronization in iteratively constructed networks in vitro. Thus, network synchronization is adjusted in area CA3 through activity-dependent remodeling of ID.
机译：神经元内在激发性（HPIE）的稳态可塑性操作以保持生理界内的网络，以应对慢性活性的慢性变化。经典上，这种形式的可塑性通过调节电压门控离子通道调节神经元的输出烧制水平。离子通道还通过塑造亚阈值和内在电位来确定各个神经元中的尖峰时序。因此，有趣的假设是HPIE还可以调节网络同步。我们在这里展示了树突毒素敏感的D型K +电流（ID）破坏了Ca3金字塔神经元中AP生成的精度，并且可以反过来限制网络同步。减小的精度由向外ID的序列介导，然后内向Na +电流。 ID的稳态下调增加了峰值时间精度和在体外迭代构建网络中的同步倾向。因此，通过ID的活动依赖性重塑在区域CA3中调整网络同步。

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