SK channels and NMDA receptors form a Ca2+-mediated feedback loop in dendritic spines Academic Article uri icon

Overview

MeSH Major

  • Calcium Signaling
  • Dendritic Spines
  • Feedback, Physiological
  • Hippocampus
  • Potassium Channels, Calcium-Activated
  • Receptors, N-Methyl-D-Aspartate

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.

publication date

  • May 2005

Research

keywords

  • Academic Article

Identity

Language

  • eng

Digital Object Identifier (DOI)

  • 10.1038/nn1449

PubMed ID

  • 15852011

Additional Document Info

start page

  • 642

end page

  • 9

volume

  • 8

number

  • 5