Spike-Time Precision and Network Synchrony Are Controlled by the Homeostatic Regulation of the D-Type Potassium Current
Spike-Time Precision and Network Synchrony Are Controlled by the Homeostatic Regulation of the D-Type Potassium Current
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DOI：
10.1523/jneurosci.0740-10.2010
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发表时间：
2010-09-22
影响因子：
5.3
通讯作者：
Debanne, Dominique
中科院分区：
文献类型：
--
作者：
Cudmore, Robert H.;Fronzaroli-Molinieres, Laure;Debanne, Dominique
神经元内在兴奋性的稳态可塑性（HPIE）可将网络维持在生理范围内，以响应活动的慢性变化。传统上，这种形式的可塑性通过电压门控离子通道的调节来调整神经元的输出放电水平。离子通道还通过塑造阈下突触和内在电位来确定单个神经元的尖峰时间。因此，一个有趣的假设是 HPIE 还可以调节网络同步。我们在此表明，树突毒素敏感的 D 型 K+ 电流 (I-D) 会破坏 CA3 锥体神经元中 AP 生成的精度，进而可能限制网络同步。精度降低是由外向 I-D 和内向 Na+ 电流的序列介导的。 I-D 的稳态下调提高了体外迭代构建网络的尖峰时间精度和同步倾向。因此，通过 I-D 的活动相关重构来调整 CA3 区域中的网络同步。
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 (I-D) 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 I-D followed by inward Na+ current. The homeostatic downregulation of I-D 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 I-D.