Downregulation of dendritic I(h) in CA1 pyramidal neurons after LTP.

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 (I(h)) in the dendrites. After HFS-induced LTP, the h-conductance (G(h)) was reduced without changing its activation. Pharmacological blockade of I(h) had no effect on LTP induction, but occluded EPSP-to-spike potentiation, an input-specific facilitation of dendritic integration. Dynamic-clamp reduction of G(h) locally in the dendrite mimicked the effects of HFS and enhanced synaptic integration in an input-selective way. We conclude that dendritic I(h) is locally downregulated after induction of nonmaximal LTP, thus facilitating integration of the potentiated input.