NKCC1-dependent GABAergic excitation drives synaptic network maturation during early hippocampal development.

Standard

NKCC1-dependent GABAergic excitation drives synaptic network maturation during early hippocampal development. / Pfeffer, Carsten K; Stein, Valentin; Keating, Damien J; Maier, Hannes; Rinke, Ilka; Rudhard, York; Hentschke, Moritz; Rune, Gabriele M.; Jentsch, Thomas J; Hübner, Christian.

in: J NEUROSCI, Jahrgang 29, Nr. 11, 11, 2009, S. 3419-3430.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

Pfeffer, CK, Stein, V, Keating, DJ, Maier, H, Rinke, I, Rudhard, Y, Hentschke, M, Rune, GM, Jentsch, TJ & Hübner, C 2009, 'NKCC1-dependent GABAergic excitation drives synaptic network maturation during early hippocampal development.', J NEUROSCI, Jg. 29, Nr. 11, 11, S. 3419-3430. <http://www.ncbi.nlm.nih.gov/pubmed/19295148?dopt=Citation>

APA

Pfeffer, C. K., Stein, V., Keating, D. J., Maier, H., Rinke, I., Rudhard, Y., Hentschke, M., Rune, G. M., Jentsch, T. J., & Hübner, C. (2009). NKCC1-dependent GABAergic excitation drives synaptic network maturation during early hippocampal development. J NEUROSCI, 29(11), 3419-3430. [11]. http://www.ncbi.nlm.nih.gov/pubmed/19295148?dopt=Citation

Vancouver

Pfeffer CK, Stein V, Keating DJ, Maier H, Rinke I, Rudhard Y et al. NKCC1-dependent GABAergic excitation drives synaptic network maturation during early hippocampal development. J NEUROSCI. 2009;29(11):3419-3430. 11.

Bibtex

@article{058f6b366bb34d5b834c5095c4516096,
title = "NKCC1-dependent GABAergic excitation drives synaptic network maturation during early hippocampal development.",
abstract = "A high intracellular chloride concentration in immature neurons leads to a depolarizing action of GABA that is thought to shape the developing neuronal network. We show that GABA-triggered depolarization and Ca2+ transients were attenuated in mice deficient for the Na-K-2Cl cotransporter NKCC1. Correlated Ca2+ transients and giant depolarizing potentials (GDPs) were drastically reduced and the maturation of the glutamatergic and GABAergic transmission in CA1 delayed. Brain morphology, synaptic density, and expression levels of certain developmental marker genes were unchanged. The expression of lynx1, a protein known to dampen network activity, was decreased. In mice deficient for the neuronal Cl(-)/HCO(3)(-) exchanger AE3, GDPs were also diminished. These data show that NKCC1-mediated Cl(-) accumulation contributes to GABAergic excitation and network activity during early postnatal development and thus facilitates the maturation of excitatory and inhibitory synapses.",
author = "Pfeffer, {Carsten K} and Valentin Stein and Keating, {Damien J} and Hannes Maier and Ilka Rinke and York Rudhard and Moritz Hentschke and Rune, {Gabriele M.} and Jentsch, {Thomas J} and Christian H{\"u}bner",
year = "2009",
language = "Deutsch",
volume = "29",
pages = "3419--3430",
journal = "J NEUROSCI",
issn = "0270-6474",
publisher = "Society for Neuroscience",
number = "11",

}

RIS

TY - JOUR

T1 - NKCC1-dependent GABAergic excitation drives synaptic network maturation during early hippocampal development.

AU - Pfeffer, Carsten K

AU - Stein, Valentin

AU - Keating, Damien J

AU - Maier, Hannes

AU - Rinke, Ilka

AU - Rudhard, York

AU - Hentschke, Moritz

AU - Rune, Gabriele M.

AU - Jentsch, Thomas J

AU - Hübner, Christian

PY - 2009

Y1 - 2009

N2 - A high intracellular chloride concentration in immature neurons leads to a depolarizing action of GABA that is thought to shape the developing neuronal network. We show that GABA-triggered depolarization and Ca2+ transients were attenuated in mice deficient for the Na-K-2Cl cotransporter NKCC1. Correlated Ca2+ transients and giant depolarizing potentials (GDPs) were drastically reduced and the maturation of the glutamatergic and GABAergic transmission in CA1 delayed. Brain morphology, synaptic density, and expression levels of certain developmental marker genes were unchanged. The expression of lynx1, a protein known to dampen network activity, was decreased. In mice deficient for the neuronal Cl(-)/HCO(3)(-) exchanger AE3, GDPs were also diminished. These data show that NKCC1-mediated Cl(-) accumulation contributes to GABAergic excitation and network activity during early postnatal development and thus facilitates the maturation of excitatory and inhibitory synapses.

AB - A high intracellular chloride concentration in immature neurons leads to a depolarizing action of GABA that is thought to shape the developing neuronal network. We show that GABA-triggered depolarization and Ca2+ transients were attenuated in mice deficient for the Na-K-2Cl cotransporter NKCC1. Correlated Ca2+ transients and giant depolarizing potentials (GDPs) were drastically reduced and the maturation of the glutamatergic and GABAergic transmission in CA1 delayed. Brain morphology, synaptic density, and expression levels of certain developmental marker genes were unchanged. The expression of lynx1, a protein known to dampen network activity, was decreased. In mice deficient for the neuronal Cl(-)/HCO(3)(-) exchanger AE3, GDPs were also diminished. These data show that NKCC1-mediated Cl(-) accumulation contributes to GABAergic excitation and network activity during early postnatal development and thus facilitates the maturation of excitatory and inhibitory synapses.

M3 - SCORING: Zeitschriftenaufsatz

VL - 29

SP - 3419

EP - 3430

JO - J NEUROSCI

JF - J NEUROSCI

SN - 0270-6474

IS - 11

M1 - 11

ER -