Hauptseite > Publikationsdatenbank > KCC2 reverse mode helps to clear postsynaptically released potassium at glutamatergic synapses |
Journal Article | FZJ-2023-03081 |
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2023
Elsevier
[New York, NY]
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Please use a persistent id in citations: doi:10.1016/j.celrep.2023.112934 doi:10.34734/FZJ-2023-03081
Abstract: Extracellular potassium [K+]o elevation during synaptic activity retrogradely modifies presynaptic release and astrocytic uptake of glutamate. Hence, local K+ clearance and replenishment mechanisms are crucial regulators of glutamatergic transmission and plasticity. Based on recordings of astrocytic inward rectifier potassium current IKir and K+-sensitive electrodes as sensors of [K+]o as well as on in silico modeling, we demonstrate that the neuronal K+-Cl- co-transporter KCC2 clears local perisynaptic [K+]o during synaptic excitation by operating in an activity-dependent reversed mode. In reverse mode, KCC2 replenishes K+ in dendritic spines and complements clearance of [K+]o, therewith attenuating presynaptic glutamate release and shortening LTP. We thus demonstrate a physiological role of KCC2 in neuron-glial interactions and regulation of synaptic signaling and plasticity through the uptake of postsynaptically released K+.
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