Premium
Components of neuronal chloride transport in rat and human neocortex
Author(s) -
Deisz Rudolf A.,
Lehmann ThomasN.,
Horn Peter,
Dehnicke Christoph,
Nitsch Robert
Publication year - 2011
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2010.201830
Subject(s) - bumetanide , gabaa receptor , biophysics , neocortex , chemistry , inhibitory postsynaptic potential , reversal potential , transporter , postsynaptic potential , chloride , intracellular , receptor , ion transporter , biochemistry , endocrinology , neuroscience , patch clamp , biology , membrane , gene , organic chemistry
Non‐technical summary The inhibitory neurotransmitter GABA activates two distinct receptors of which the GABA A receptor is mainly a Cl − conducting ion channel. The proper functioning of inhibition at the GABA A receptor depends on the ionic gradient prevailing during receptor activation, and in epilepsy there is an aberrant Cl − gradient. Using rat and human cortical neurones and pharmacological inhibitors, we calculated the contributions of neuronal Cl − extrusion by the Na + –K + –2Cl − transporter NKCC1, the K + ‐coupled Cl − transporter KCC2 and the voltage‐gated Cl − channel ClC2. We found that KCC2 is the major route of Cl − extrusion and that reduced KCC2 Cl − extrusion is likely to be the initial step of disturbed Cl − regulation. The results contribute to our understanding of epilepsy.