Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-5757
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dc.contributor.authorKolbaev, Sergey N.-
dc.contributor.authorMohapatra, Namrata-
dc.contributor.authorChen, Rongqing-
dc.contributor.authorLombardi, Aniello-
dc.contributor.authorStaiger, Jochen F.-
dc.contributor.authorLuhmann, Heiko J.-
dc.contributor.authorJedlicka, Peter-
dc.contributor.authorKilb, Werner-
dc.date.accessioned2021-04-22T10:12:48Z-
dc.date.available2021-04-22T10:12:48Z-
dc.date.issued2020-
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/5766-
dc.description.abstractActivation of GABAA receptors causes in immature neurons a functionally relevant decrease in the intracellular Cl− concentration ([Cl−]i), a process termed ionic plasticity. Amount and duration of ionic plasticity depends on kinetic properties of [Cl−]i homeostasis. In order to characterize the capacity of Cl− accumulation and to quantify the effect of persistent GABAergic activity on [Cl−]i, we performed gramicidin-perforated patch-clamp recordings from CA3 pyramidal neurons of immature (postnatal day 4–7) rat hippocampal slices. These experiments revealed that inhibition of NKCC1 decreased [Cl−]i toward passive distribution with a time constant of 381 s. In contrast, active Cl− accumulation occurred with a time constant of 155 s, corresponding to a rate of 15.4 µM/s. Inhibition of phasic GABAergic activity had no significant effect on steady state [Cl−]i. Inhibition of tonic GABAergic currents induced a significant [Cl−]i increase by 1.6 mM, while activation of tonic extrasynaptic GABAA receptors with THIP significantly reduced [Cl−]i.. Simulations of neuronal [Cl−]i homeostasis supported the observation, that basal levels of synaptic GABAergic activation do not affect [Cl−]i. In summary, these results indicate that active Cl−-uptake in immature hippocampal neurons is sufficient to maintain stable [Cl−]i at basal levels of phasic and to some extent also to compensate tonic GABAergic activity.en_GB
dc.language.isoengde
dc.rightsCC BY*
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/*
dc.subject.ddc610 Medizinde_DE
dc.subject.ddc610 Medical sciencesen_GB
dc.titleNKCC-1 mediated Cl− uptake in immature CA3 pyramidal neurons is sufficient to compensate phasic GABAergic inputsen_GB
dc.typeZeitschriftenaufsatzde
dc.identifier.doihttp://doi.org/10.25358/openscience-5757-
jgu.type.dinitypearticleen_GB
jgu.type.versionPublished versionde
jgu.type.resourceTextde
jgu.organisation.departmentFB 04 Medizinde
jgu.organisation.number2700-
jgu.organisation.nameJohannes Gutenberg-Universität Mainz-
jgu.rights.accessrightsopenAccess-
jgu.journal.titleScientific reportsde
jgu.journal.volume10de
jgu.pages.alternative18399de
jgu.publisher.year2020-
jgu.publisher.nameMacmillan Publishers Limited, part of Springer Naturede
jgu.publisher.placeLondonde
jgu.publisher.urihttps://doi.org/10.1038/s41598-020-75382-1de
jgu.publisher.issn2045-2322de
jgu.organisation.placeMainz-
jgu.subject.ddccode610de
jgu.publisher.doi10.1038/s41598-020-75382-1
jgu.organisation.rorhttps://ror.org/023b0x485
Appears in collections:JGU-Publikationen

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