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Dendritic K + channels contribute to spike-timing dependent long-term potentiation in hippocampal pyramidal neurons

2002; National Academy of Sciences; Volume: 99; Issue: 12 Linguagem: Inglês

10.1073/pnas.122210599

1091-6490

Shigeo Watanabe, Dax A. Hoffman, Michele Migliore, Daniel Johnston,

Photoreceptor and optogenetics research

We investigated the role of A-type K + channels for the induction of long-term potentiation (LTP) of Schaffer collateral inputs to hippocampal CA1 pyramidal neurons. When low-amplitude excitatory postsynaptic potentials (EPSPs) were paired with two postsynaptic action potentials in a theta-burst pattern, N -methyl- d -aspartate (NMDA)-receptor-dependent LTP was induced. The amplitudes of the back-propagating action potentials were boosted in the dendrites only when they were coincident with the EPSPs. Mitogen-activated protein kinase (MAPK) inhibitors PD 098059 or U0126 shifted the activation of dendritic K + channels to more hyperpolarized potentials, reduced the boosting of dendritic action potentials by EPSPs, and suppressed the induction of LTP. These results support the hypothesis that dendritic K + channels and the boosting of back-propagating action potentials contribute to the induction of LTP in CA1 neurons.