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Coupled Activity‐dependent Trafficking of SK2 Channels and Glutamate Receptors
Author(s) -
Lin Mike T,
Lujan Rafael,
Watanabe Masahiko,
Frerking Matthew E,
Adelman John P,
Maylie James
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.810.3
Subject(s) - ampa receptor , excitatory postsynaptic potential , long term potentiation , nmda receptor , postsynaptic density , neuroscience , postsynaptic potential , glutamate receptor , chemistry , microbiology and biotechnology , inhibitory postsynaptic potential , biology , receptor , biochemistry
Small conductance Ca 2+ activated K + type 2 (SK2) channels are expressed in the postsynaptic density (PSD) of CA1 neurons where they are activated by synaptically evoked Ca 2+ influx, providing a local inhibitory current. Upon the induction of long‐term potentiation (LTP), synaptic SK2 channels undergo protein kinase A (PKA)‐dependent endocytosis, thus contributing to the increased excitatory postsynaptic potential (EPSP). Under basal conditions, SK2 channels and α‐amino‐3‐hydroxyl‐5‐methyl‐4‐isoxazole‐propionate receptors (AMPAr) populate distinct sets of endosomes. Surprisingly, inhibiting LTP‐dependent AMPAr exocytosis also blocks SK2 channel endocytosis. Following LTP and internalization, SK2 channels repopulate the PSD within ~2 hours. This time course is similar to the accumulation of N‐methyl‐D‐aspartate receptors (NMDAr) that rebalances the AMPA‐to‐NMDA ratio, and during this time SK2 channels and NMDAr co‐localize to the same vesicles. Thus, the trafficking of spine SK2 channels and the two subtypes of glutamate receptors are tightly and differentially coupled in response to LTP.