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

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

    Universidad de La Laguna

    San Cristobal de La Laguna, España

    ROR https://ror.org/01r9z8p25

Revista:
Proceedings of the National Academy of Sciences

ISSN: 0027-8424 1091-6490

Año de publicación: 2021

Volumen: 118

Número: 35

Páginas: e2107026118

Tipo: Artículo

DOI: 10.1073/PNAS.2107026118 GOOGLE SCHOLAR

Otras publicaciones en: Proceedings of the National Academy of Sciences

Resumen

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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