Journal Article FZJ-2023-03081

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KCC2 reverse mode helps to clear postsynaptically released potassium at glutamatergic synapses

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2023
Elsevier [New York, NY]

Cell reports 42(8), 112934 - () [10.1016/j.celrep.2023.112934]

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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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Note: 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).

Contributing Institute(s):
  1. Molekular- und Zellphysiologie (IBI-1)
Research Program(s):
  1. 5243 - Information Processing in Distributed Systems (POF4-524) (POF4-524)

Appears in the scientific report 2023
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Open Access

 Datensatz erzeugt am 2023-08-17, letzte Änderung am 2024-02-26


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