NpgRj_NN_1449 642..649
نویسندگان
چکیده
Small-conductance Ca21-activated K1 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 Ca21 influx within individual spines. SK channels are tightly coupled to synaptically activated Ca21 sources, and their activity reduces the amplitude of NMDAR-dependent Ca21 transients. These effects are mediated by a feedback loop within the spine head; during an excitatory postsynaptic potential (EPSP), Ca21 influx opens SK channels that provide a local shunting current to reduce the EPSP and promote rapid Mg21 block of the NMDAR. Thus, blocking SK channels facilitates the induction of long-term potentiation by enhancing NMDAR-dependent Ca21 signals within dendritic spines.
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