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

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

Research output: Contribution to journalArticle

299 Citations (Scopus)

Abstract

Small-conductance Ca2+-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 Ca2+ influx within individual spines. SK channels are tightly coupled to synaptically activated Ca2+ sources, and their activity reduces the amplitude of NMDAR-dependent Ca2+ transients. These effects are mediated by a feedback loop within the spine head; during an excitatory postsynaptic potential (EPSP), Ca2+ influx opens SK channels that provide a local shunting current to reduce the EPSP and promote rapid Mg2+ block of the NMDAR. Thus, blocking SK channels facilitates the induction of long-term potentiation by enhancing NMDAR-dependent Ca2+ signals within dendritic spines.

Original languageEnglish (US)
Pages (from-to)642-649
Number of pages8
JournalNature Neuroscience
Volume8
Issue number5
DOIs
StatePublished - May 2005

Fingerprint

Calcium-Activated Potassium Channels
Dendritic Spines
N-Methyl-D-Aspartate Receptors
Excitatory Postsynaptic Potentials
Photons
Spine
Synaptic Potentials
Neuronal Plasticity
Long-Term Potentiation
Evoked Potentials
Confocal Microscopy
Synapses
Glutamic Acid
Lasers

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Ngo-Anh, T. J., Bloodgood, B. L., Lin, M., Sabatini, B. L., Maylie, J., & Adelman, J. (2005). SK channels and NMDA receptors form a Ca2+-mediated feedback loop in dendritic spines. Nature Neuroscience, 8(5), 642-649. https://doi.org/10.1038/nn1449

SK channels and NMDA receptors form a Ca2+-mediated feedback loop in dendritic spines. / Ngo-Anh, Thu Jennifer; Bloodgood, Brenda L.; Lin, Michael; Sabatini, Bernardo L.; Maylie, James; Adelman, John.

In: Nature Neuroscience, Vol. 8, No. 5, 05.2005, p. 642-649.

Research output: Contribution to journalArticle

Ngo-Anh, TJ, Bloodgood, BL, Lin, M, Sabatini, BL, Maylie, J & Adelman, J 2005, 'SK channels and NMDA receptors form a Ca2+-mediated feedback loop in dendritic spines', Nature Neuroscience, vol. 8, no. 5, pp. 642-649. https://doi.org/10.1038/nn1449
Ngo-Anh, Thu Jennifer ; Bloodgood, Brenda L. ; Lin, Michael ; Sabatini, Bernardo L. ; Maylie, James ; Adelman, John. / SK channels and NMDA receptors form a Ca2+-mediated feedback loop in dendritic spines. In: Nature Neuroscience. 2005 ; Vol. 8, No. 5. pp. 642-649.
@article{5d5b29cb9f7841d5bc02675abfce9549,
title = "SK channels and NMDA receptors form a Ca2+-mediated feedback loop in dendritic spines",
abstract = "Small-conductance Ca2+-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 Ca2+ influx within individual spines. SK channels are tightly coupled to synaptically activated Ca2+ sources, and their activity reduces the amplitude of NMDAR-dependent Ca2+ transients. These effects are mediated by a feedback loop within the spine head; during an excitatory postsynaptic potential (EPSP), Ca2+ influx opens SK channels that provide a local shunting current to reduce the EPSP and promote rapid Mg2+ block of the NMDAR. Thus, blocking SK channels facilitates the induction of long-term potentiation by enhancing NMDAR-dependent Ca2+ signals within dendritic spines.",
author = "Ngo-Anh, {Thu Jennifer} and Bloodgood, {Brenda L.} and Michael Lin and Sabatini, {Bernardo L.} and James Maylie and John Adelman",
year = "2005",
month = "5",
doi = "10.1038/nn1449",
language = "English (US)",
volume = "8",
pages = "642--649",
journal = "Nature Neuroscience",
issn = "1097-6256",
publisher = "Nature Publishing Group",
number = "5",

}

TY - JOUR

T1 - SK channels and NMDA receptors form a Ca2+-mediated feedback loop in dendritic spines

AU - Ngo-Anh, Thu Jennifer

AU - Bloodgood, Brenda L.

AU - Lin, Michael

AU - Sabatini, Bernardo L.

AU - Maylie, James

AU - Adelman, John

PY - 2005/5

Y1 - 2005/5

N2 - Small-conductance Ca2+-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 Ca2+ influx within individual spines. SK channels are tightly coupled to synaptically activated Ca2+ sources, and their activity reduces the amplitude of NMDAR-dependent Ca2+ transients. These effects are mediated by a feedback loop within the spine head; during an excitatory postsynaptic potential (EPSP), Ca2+ influx opens SK channels that provide a local shunting current to reduce the EPSP and promote rapid Mg2+ block of the NMDAR. Thus, blocking SK channels facilitates the induction of long-term potentiation by enhancing NMDAR-dependent Ca2+ signals within dendritic spines.

AB - Small-conductance Ca2+-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 Ca2+ influx within individual spines. SK channels are tightly coupled to synaptically activated Ca2+ sources, and their activity reduces the amplitude of NMDAR-dependent Ca2+ transients. These effects are mediated by a feedback loop within the spine head; during an excitatory postsynaptic potential (EPSP), Ca2+ influx opens SK channels that provide a local shunting current to reduce the EPSP and promote rapid Mg2+ block of the NMDAR. Thus, blocking SK channels facilitates the induction of long-term potentiation by enhancing NMDAR-dependent Ca2+ signals within dendritic spines.

UR - http://www.scopus.com/inward/record.url?scp=17844385283&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=17844385283&partnerID=8YFLogxK

U2 - 10.1038/nn1449

DO - 10.1038/nn1449

M3 - Article

C2 - 15852011

AN - SCOPUS:17844385283

VL - 8

SP - 642

EP - 649

JO - Nature Neuroscience

JF - Nature Neuroscience

SN - 1097-6256

IS - 5

ER -