SK2 channel plasticity contributes to LTP at Schaffer collateral-CA1 synapses Academic Article uri icon

Overview

MeSH Major

  • Hippocampus
  • Long-Term Potentiation
  • Nerve Fibers
  • Neuronal Plasticity
  • Small-Conductance Calcium-Activated Potassium Channels
  • Synapses

abstract

  • Long-term potentiation (LTP) of synaptic strength at Schaffer collateral synapses has largely been attributed to changes in the number and biophysical properties of AMPA receptors (AMPARs). Small-conductance Ca(2+)-activated K(+) channels (SK2 channels) are functionally coupled with NMDA receptors (NMDARs) in CA1 spines such that their activity modulates the shape of excitatory postsynaptic potentials (EPSPs) and increases the threshold for induction of LTP. Here we show that LTP induction in mouse hippocampus abolishes SK2 channel activity in the potentiated synapses. This effect is due to SK2 channel internalization from the postsynaptic density (PSD) into the spine. Blocking PKA or cell dialysis with a peptide representing the C-terminal domain of SK2 that contains three known PKA phosphorylation sites blocks the internalization of SK2 channels after LTP induction. Thus the increase in AMPARs and the decrease in SK2 channels combine to produce the increased EPSP underlying LTP.

publication date

  • February 2008

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed Central ID

  • PMC2613806

Digital Object Identifier (DOI)

  • 10.1038/nn2041

PubMed ID

  • 18204442

Additional Document Info

start page

  • 170

end page

  • 7

volume

  • 11

number

  • 2