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SK2 channel plasticity contributes to LTP at Schaffer collateral-CA1 synapses
Mike T Lin1, Rafael Luján, Masahiko Watanabe
1Vollum Institute, Oregon Health & Science University, Portland, Oregon 97239, USA.
Nature Neuroscience
|January 22, 2008
Summary
Long-term potentiation (LTP) involves changes in AMPA receptors (AMPARs) and a decrease in small-conductance Ca(2+)-activated K(+) channels (SK2 channels). LTP induction causes SK2 channel internalization, contributing to enhanced synaptic strength.
Area of Science:
- Neuroscience
- Synaptic Plasticity
- Molecular Biology
Background:
- Long-term potentiation (LTP) enhances synaptic strength, primarily linked to AMPA receptor (AMPAR) changes.
- Small-conductance Ca(2+)-activated K(+) channels (SK2 channels) regulate excitatory postsynaptic potentials (EPSPs) and LTP induction thresholds.
- SK2 channels are functionally coupled with NMDA receptors (NMDARs) in CA1 spines.
Purpose of the Study:
- To investigate the role of SK2 channels in LTP at Schaffer collateral synapses.
- To elucidate the mechanism by which SK2 channel activity is modulated during LTP induction.
- To understand the combined contribution of AMPARs and SK2 channels to synaptic potentiation.
Main Methods:
- Electrophysiological recordings in mouse hippocampus.
- Investigating SK2 channel activity and localization during LTP.
- Utilizing PKA inhibition and peptide dialysis to block SK2 channel internalization.
Main Results:
- LTP induction leads to the abolition of SK2 channel activity in potentiated synapses.
- SK2 channel internalization from the postsynaptic density into the spine underlies this activity loss.
- Inhibition of PKA or disruption of SK2 C-terminal domain prevents internalization.
Conclusions:
- LTP involves both an increase in AMPARs and a decrease in SK2 channel function.
- SK2 channel internalization, regulated by PKA, is a key event in synaptic potentiation.
- The interplay between AMPARs and SK2 channels determines the enhanced EPSP characteristic of LTP.
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