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Journal Article

Dendritic potassium channels 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

Johnston, D., Hoffman, D. A., Magee, J. C., Poolos, N. P., Watanabe, S., Colbert, C. M., et al. (2000). Dendritic potassium channels in hippocampal pyramidal neurons. The Journal of Physiology - London, 525(1), 75-81. doi:10.1111/j.1469-7793.2000.00075.x.


Cite as: https://hdl.handle.net/21.11116/0000-0002-4727-3
Abstract
Potassium channels located in the dendrites of hippocampal CA1 pyramidal neurons control the shape and amplitude of back-propagating action potentials, the amplitude of excitatory postsynaptic potentials and dendritic excitability. Non-uniform gradients in the distribution of potassium channels in the dendrites make the dendritic electrical properties markedly different from those found in the soma. For example, the influence of a fast, calcium-dependent potassium current on action potential repolarization is progressively reduced in the first 150 micrometer of the apical dendrites, so that action potentials recorded farther than 200 micrometer from the soma have no fast after-hyperpolarization and are wider than those in the soma. The peak amplitude of back-propagating action potentials is also progressively reduced in the dendrites because of the increasing density of a transient potassium channel with distance from the soma. The activation of this channel can be reduced by the activity of a number of protein kinases as well as by prior depolarization. The depolarization from excitatory postsynaptic potentials (EPSPs) can inactivate these A-type K+ channels and thus lead to an increase in the amplitude of dendritic action potentials, provided the EPSP and the action potentials occur within the appropriate time window. This time window could be in the order of 15 ms and may play a role in long-term potentiation induced by pairing EPSPs and back-propagating action potentials.