Title: SK channels and NMDA receptors form a Ca2+-mediated feedback loop in dendritic spines.

Authors: Thu Jennifer Ngo-Anh, Brenda L Bloodgood, Michael Lin, Bernardo L Sabatini, James Maylie, John P Adelman

Journal, date & volume: Nat. Neurosci., 2005 May , 8, 642-9

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/15852011

Abstract
Small-conductance Ca(2+)-activated K(+) channels (SK channels) influence the induction of synaptic plasticity at hippocampal CA3-CA1 synapses. We find that in mice, SK channels are localized to dendritic spines, and their activity reduces the amplitude of evoked synaptic potentials in an NMDA receptor (NMDAR)-dependent manner. Using combined two-photon laser scanning microscopy and two-photon laser uncaging of glutamate, we show that SK channels regulate NMDAR-dependent Ca(2+) influx within individual spines. SK channels are tightly coupled to synaptically activated Ca(2+) sources, and their activity reduces the amplitude of NMDAR-dependent Ca(2+) transients. These effects are mediated by a feedback loop within the spine head; during an excitatory postsynaptic potential (EPSP), Ca(2+) influx opens SK channels that provide a local shunting current to reduce the EPSP and promote rapid Mg(2+) block of the NMDAR. Thus, blocking SK channels facilitates the induction of long-term potentiation by enhancing NMDAR-dependent Ca(2+) signals within dendritic spines.