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, Vol. 29, No. 11, 11, 2009, p. 3419-3430.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
Harvard
APA
Vancouver
Bibtex
}
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 -