NMDA receptor–BK channel coupling regulates synaptic plasticity in the barrel cortex
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Gonzalez-Hernandez, Alberto J.
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Giraldez, Teresa
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Maglio, Laura E.
- Rivero-Pérez, Belinda
- Bartolomé-Martín, David
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Gómez, Ricardo
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1
Universidad de La Laguna
info
ISSN: 0027-8424, 1091-6490
Año de publicación: 2021
Volumen: 118
Número: 35
Páginas: e2107026118
Tipo: Artículo
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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