Home > Publications database > KCC2 reverse mode helps to clear postsynaptically released potassium at glutamatergic synapses > print |
001 | 1010486 | ||
005 | 20240226075454.0 | ||
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100 | 1 | _ | |a Byvaltcev, Egor |b 0 |
245 | _ | _ | |a KCC2 reverse mode helps to clear postsynaptically released potassium at glutamatergic synapses |
260 | _ | _ | |a [New York, NY] |c 2023 |b Elsevier |
336 | 7 | _ | |a article |2 DRIVER |
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500 | _ | _ | |a This project has received funding from the EuropeanResearch Council (ERC) under the Union’s Horizon 2020 research an innovation program (grant agreement no. 864243) and from the Einstein FoundationBerlin (EP-2021-621). |
520 | _ | _ | |a 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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700 | 1 | _ | |a Behbood, Mahraz |b 1 |
700 | 1 | _ | |a Schleimer, Jan-Hendrik |b 2 |
700 | 1 | _ | |a Gensch, Thomas |0 P:(DE-Juel1)131924 |b 3 |u fzj |
700 | 1 | _ | |a Semyanov, Alexey |b 4 |
700 | 1 | _ | |a Schreiber, Susanne |b 5 |
700 | 1 | _ | |a Strauss, Ulf |0 0000-0002-1534-6624 |b 6 |e Corresponding author |
773 | _ | _ | |a 10.1016/j.celrep.2023.112934 |g Vol. 42, no. 8, p. 112934 - |0 PERI:(DE-600)2649101-1 |n 8 |p 112934 - |t Cell reports |v 42 |y 2023 |x 2211-1247 |
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