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

This title appears in the Scientific Report : 2023

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

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...

Personal Name(s):	Byvaltcev, Egor
	Behbood, Mahraz / Schleimer, Jan-Hendrik / Gensch, Thomas / Semyanov, Alexey / Schreiber, Susanne / Strauss, Ulf (Corresponding author)
Contributing Institute:	Molekular- und Zellphysiologie; IBI-1
Published in:	Cell reports, 42 (2023) 8, S. 112934 -
Imprint:	[New York, NY] Elsevier 2023
DOI:	10.34734/FZJ-2023-03081
DOI:	10.1016/j.celrep.2023.112934
Document Type:	Journal Article
Research Program:	Information Processing in Distributed Systems
Link:	Get full text OpenAccess
	Publikationsportal JuSER

Please use the identifier: http://dx.doi.org/10.34734/FZJ-2023-03081 in citations.
Please use the identifier: http://dx.doi.org/10.1016/j.celrep.2023.112934 in citations.

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+.