Downregulation of dendritic Ih in CA1 pyramidal neurons after LTP
Downregulation of dendritic Ih in CA1 pyramidal neurons after LTP
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DOI：
10.1523/jneurosci.1411-08.2008
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发表时间：
2008-08-20
影响因子：
5.3
通讯作者：
Debanne, Dominique
中科院分区：
文献类型：
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作者：
Campanac, Emilie;Daoudal, Gael;Debanne, Dominique
超极化激活的(H)通道在树突状细胞功能中占有中心地位。尽管已经证明这些通道在大的去极化后被上调以减少树突状细胞的激发，但尚不清楚它们是否也支持其他形式的长期可塑性。在这里，我们发现由theta-Burst配对引起的几乎最大长时程增强(LTP)导致CA1锥体神经元h-通道活动的上调。相反，由脉冲时间依赖性可塑性或高频刺激(HFS)诱导的适度LTP下调树突中的h-电流(Ih)。在HFS诱导LTP后，h-电导(G(H))降低，但不改变其活性。药物阻断iH对LTP的诱导没有影响，但阻断了EPSP到棘波的增强，这是一种输入特异性的促进树突整合的机制。在树突局部动态钳制GH的作用模仿了HFS的作用，并以一种输入选择性的方式增强了突触整合。我们的结论是，在非最大LTP诱导后，树突Ih在局部下调，从而促进了增强输入的整合。
Hyperpolarization-activated (h)-channels occupy a central position in dendritic function. Although it has been demonstrated that these channels are upregulated after large depolarizations to reduce dendritic excitation, it is not clear whether they also support other forms of long-term plasticity. We show here that nearly maximal long-term potentiation (LTP) induced by theta-burst pairing produced upregulation in h-channel activity in CA1 pyramidal neurons. In contrast, moderate LTP induced by spike-timing-dependent plasticity or high-frequency stimulation (HFS) downregulated the h-current (Ih) in the dendrites. After HFS-induced LTP, the h-conductance (G(h)) was reduced without changing its activation. Pharmacological blockade of Ih had no effect on LTP induction, but occluded EPSP-to-spike potentiation, an input-specific facilitation of dendritic integration. Dynamic-clamp reduction of Gh locally in the dendrite mimicked the effects of HFS and enhanced synaptic integration in an input-selective way. We conclude that dendritic Ih is locally downregulated after induction of nonmaximal LTP, thus facilitating integration of the potentiated input.