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

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

doi:10.1073/pnas.122210599

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

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Hoffman, Dax A.
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

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Citation

Watanabe, S., Hoffman, D. A., Migliore, M., & Johnston, D. (2002). Dendritic K+ channels contribute to spike-timing dependent long-term potentiation in hippocampal pyramidal neurons. Proceedings of the National Academy of Sciences of the United States of America, 99(12), 8366-8371. doi:10.1073/pnas.122210599.

Cite as: https://hdl.handle.net/21.11116/0000-0001-EF7E-6

Abstract

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.