TY  - JOUR
AU  - Byvaltcev, Egor
AU  - Behbood, Mahraz
AU  - Schleimer, Jan-Hendrik
AU  - Gensch, Thomas
AU  - Semyanov, Alexey
AU  - Schreiber, Susanne
AU  - Strauss, Ulf
TI  - KCC2 reverse mode helps to clear postsynaptically released potassium at glutamatergic synapses
JO  - Cell reports
VL  - 42
IS  - 8
SN  - 2211-1247
CY  - [New York, NY]
PB  - Elsevier
M1  - FZJ-2023-03081
SP  - 112934 -
PY  - 2023
N1  - 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).
AB  - 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+.
LB  - PUB:(DE-HGF)16
C6  - 37537840
UR  - <Go to ISI:>//WOS:001051595700001
DO  - DOI:10.1016/j.celrep.2023.112934
UR  - https://juser.fz-juelich.de/record/1010486
ER  -