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Potassium Channels: Newly Found Players in Synaptic Plasticity

^* To whom correspondence should be addressed. E-mail: hoffmand{at}mail.nih.gov.

	Abstract

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 XX(X):xx–xx, XXXX. DOI: 10.1177/1073858408315041

First published on April 15, 2008, doi:10.1177/1073858408315041

The Neuroscientist 2008;14:276.

A more recent version of this article appeared on June 1, 2008


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