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This version was published on June 1, 2008
The Neuroscientist, Vol. 14, No. 3, 276-286 (2008)
DOI: 10.1177/1073858408315041

Potassium Channels: Newly Found Players in Synaptic Plasticity

Jinhyun Kim

Molecular Neurophysiology and Biophysics Unit, Laboratory of Cellular and Synaptic Neurophysiology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, kimj{at}janelia.hhmi.org

Dax A. Hoffman

Molecular Neurophysiology and Biophysics Unit, Laboratory of Cellular and Synaptic Neurophysiology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, hoffmand{at}mail.nih.gov

One of the major issues for modern neuroscience research concerns the molecular and cellular mechanisms that underlie the acquisition, storage, and recollection of memories by the brain. Regulation of the strength of individual synaptic inputs (synaptic plasticity) has, for decades, been the front-running candidate mechanism for cellular information storage, with some direct supporting evidence recently obtained. Research into the molecular mechanisms responsible for changing synaptic strength has, to date, primarily focused on trafficking and properties of the neurotransmitter receptors themselves (AMPARs and NMDARs). However, recent evidence indicates that, subsequent to receptor activation, synaptic inputs are subject to regulation by synaptically located K+ channels. It is therefore critical to understand the biophysical properties and subcellular localization (density and distribution) of these channels and how their properties are modulated. Here we will review recent findings showing that two different classes of K+ channels (A-type and small conductance, Ca2+ -activated K+ channels), beyond their traditional role in regulating action potential firing, contribute to the regulation of synaptic strength in the hippocampus. In addition, we discuss how modulation of these channels' properties and expression might contribute to synaptic plasticity. NEUROSCIENTIST 14(3):276–286, 2008. DOI: 10.1177/1073858408315041

Key Words: Potassium channel • Kv4.2 • SK • Trafficking • Synaptic plasticity


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R. S. Hammond, L. Lin, M. S. Sidorov, A. M. Wikenheiser, and D. A. Hoffman
Protein Kinase A Mediates Activity-Dependent Kv4.2 Channel Trafficking
J. Neurosci., July 23, 2008; 28(30): 7513 - 7519.
[Abstract] [Full Text] [PDF]