NMDA receptor–BK channel coupling regulates synaptic plasticity in the barrel cortex

  1. Gómez, Ricardo 1
  2. Maglio, Laura E. 1
  3. Gonzalez-Hernandez, Alberto J. 1
  4. Rivero-Pérez, Belinda 1
  5. Bartolomé-Martín, David 1
  6. Giraldez, Teresa 1
  1. 1 Universidad de La Laguna
    info

    Universidad de La Laguna

    San Cristobal de La Laguna, España

    GRID grid.10041.34

Journal:
Proceedings of the National Academy of Sciences

ISSN: 0027-8424

Year of publication: 2021

Volume: 118

Issue: 35

Pages: e2107026118

Type: Article

Export: RIS
DOI: 10.1073/pnas.2107026118 GOOGLE SCHOLAR

Metrics

Cited by

  • Scopus Cited by: 0 (05-10-2021)

JCR (Journal Impact Factor)

(Indicator corresponding to the last year available on this portal, year 2020)
  • Year 2020
  • Journal Impact Factor: 11.205
  • Best Quartile: Q1
  • Area: MULTIDISCIPLINARY SCIENCES Quartile: Q1 Rank in area: 8/73 (Ranking edition: SCIE)

SCImago Journal Rank

(Indicator corresponding to the last year available on this portal, year 2020)
  • Year 2020
  • SJR Journal Impact: 5.011
  • Best Quartile: Q1
  • Area: Multidisciplinary Quartile: Q1 Rank in area: 4/135

CIRC

  • Social Sciences: C

CiteScore

(Indicator corresponding to the last year available on this portal, year 2020)
  • Year 2020
  • CiteScore of the Journal : 15.6
  • Area: Multidisciplinary Percentile: 96

Journal Citation Indicator (JCI)

(Indicator corresponding to the last year available on this portal, year 2020)
  • Year 2020
  • Journal Citation Indicator (JCI): 2.04
  • Best Quartile: Q1
  • Area: MULTIDISCIPLINARY SCIENCES Quartile: Q1 Rank in area: 7/128

Abstract

Postsynaptic N-methyl-D-aspartate receptors (NMDARs) are crucial mediators of synaptic plasticity due to their ability to act as coincidence detectors of presynaptic and postsynaptic neuronal activity. However, NMDARs exist within the molecular context of a variety of postsynaptic signaling proteins, which can fine-tune their function. Here, we describe a form of NMDAR suppression by large-conductance Ca2+- and voltage-gated K+ (BK) channels in the basal dendrites of a subset of barrel cortex layer 5 pyramidal neurons. We show that NMDAR activation increases intracellular Ca2+ in the vicinity of BK channels, thus activating K+ efflux and strong negative feedback inhibition. We further show that neurons exhibiting such NMDAR–BK coupling serve as high-pass filters for incoming synaptic inputs, precluding the induction of spike timing–dependent plasticity. Together, these data suggest that NMDAR-localized BK channels regulate synaptic integration and provide input-specific synaptic diversity to a thalamocortical circuit.

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