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

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http://pubman.mpdl.mpg.de/cone/persons/resource/persons123453

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

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Zitation

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.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-0019-9F5E-7
Zusammenfassung
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