SUMMARY
Postsynaptic N-methyl-D-aspartate receptors (NMDAR) are crucial elements in excitatory synaptic transmission and plasticity due to their role as coincidence detectors of presynaptic and postsynaptic neuronal activity. NMDAR activation is expected to have profound impact in synapse and circuit function, but such activity is not isolated. Here we describe a selective and novel suppression of NMDAR activity by large-conductance Ca2+- and voltage-gated K+ channels (BK) in basal dendrites of barrel cortex layer 5 pyramidal neurons (BC-L5PN). GluN2A- and GluN2B-containing NMDAR show functional coupling to closely located BK channels, where NMDAR activation provides the Ca2+ increase required for BK function. BK-dependent membrane repolarization constitutes a negative feedback mechanism on NMDAR-mediated excitatory stimuli, which distinctively modulates synaptic transmission and long-term plasticity. Accordingly, BC-L5PN exhibiting close NMDAR-BK coupling work as a high-pass filter for incoming afferent inputs, suggesting that BK channels can regulate synaptic input integration to an unexpected extent.
Competing Interest Statement
The authors have declared no competing interest.
Footnotes
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