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001010486 1001_ $$aByvaltcev, Egor$$b0
001010486 245__ $$aKCC2 reverse mode helps to clear postsynaptically released potassium at glutamatergic synapses
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001010486 500__ $$aThis 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).
001010486 520__ $$aExtracellular potassium [K+]o elevation during synaptic activity retrogradely modifies presynaptic release and astrocytic uptake of glutamate. Hence, local K+ clearance and replenishment mechanisms are crucial regulators of glutamatergic transmission and plasticity. Based on recordings of astrocytic inward rectifier potassium current IKir and K+-sensitive electrodes as sensors of [K+]o as well as on in silico modeling, we demonstrate that the neuronal K+-Cl- co-transporter KCC2 clears local perisynaptic [K+]o during synaptic excitation by operating in an activity-dependent reversed mode. In reverse mode, KCC2 replenishes K+ in dendritic spines and complements clearance of [K+]o, therewith attenuating presynaptic glutamate release and shortening LTP. We thus demonstrate a physiological role of KCC2 in neuron-glial interactions and regulation of synaptic signaling and plasticity through the uptake of postsynaptically released K+.
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001010486 7001_ $$aBehbood, Mahraz$$b1
001010486 7001_ $$aSchleimer, Jan-Hendrik$$b2
001010486 7001_ $$0P:(DE-Juel1)131924$$aGensch, Thomas$$b3$$ufzj
001010486 7001_ $$aSemyanov, Alexey$$b4
001010486 7001_ $$aSchreiber, Susanne$$b5
001010486 7001_ $$00000-0002-1534-6624$$aStrauss, Ulf$$b6$$eCorresponding author
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