Article abstract


Nature Neuroscience 11, 170 - 177 (2008)
Published online: 20 January 2008 | doi:10.1038/nn2041

SK2 channel plasticity contributes to LTP at Schaffer collateral–CA1 synapses

Mike T Lin1,5, Rafael Luján2,5, Masahiko Watanabe3, John P Adelman1 & James Maylie4


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 Ca2+-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.

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  1. Vollum Institute, Oregon Health & Science University, Portland, Oregon 97239, USA.
  2. Departamento de Ciencias Médicas, Universidad de Castilla–La Mancha, Albacete, Spain, 02006.
  3. Department of Anatomy, Hokkaido University School of Medicine, Sapporo 060-8638, Japan.
  4. Department of Obstetrics and Gynecology, Oregon Health & Science University, Portland, Oregon 97239, USA.
  5. These authors contributed equally to this work.

Correspondence to: John P Adelman1 e-mail: adelman@ohsu.edu

Correspondence to: James Maylie4 e-mail: mayliej@ohsu.edu



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