PT  - JOURNAL ARTICLE
AU  - Jürgen Graf
AU  - Chuanqiang Zhang
AU  - Stephan Lawrence Marguet
AU  - Tanja Herrmann
AU  - Tom Flossmann
AU  - Robin Hinsch
AU  - Vahid Rahmati
AU  - Madlen Guenther
AU  - Christiane Frahm
AU  - Anja Urbach
AU  - Ricardo Melo Neves
AU  - Otto W. Witte
AU  - Stefan J. Kiebel
AU  - Dirk Isbrandt
AU  - Christian A. Hübner
AU  - Knut Holthoff
AU  - Knut Kirmse
TI  - Intraneuronal chloride accumulation via NKCC1 is not essential for hippocampal network development <em>in vivo</em>
AID  - 10.1101/2020.07.13.200014
DP  - 2020 Jan 01
TA  - bioRxiv
PG  - 2020.07.13.200014
4099  - http://biorxiv.org/content/early/2020/07/13/2020.07.13.200014.short
4100  - http://biorxiv.org/content/early/2020/07/13/2020.07.13.200014.full
AB  - NKCC1 is the primary transporter mediating chloride uptake in immature principal neurons, but its role in the development of in vivo network dynamics and cognitive abilities remains unknown. Here, we address the function of NKCC1 in developing mice using electrophysiological, optical and behavioral approaches. We report that NKCC1 deletion from telencephalic glutamatergic neurons decreases in-vitro excitatory GABA actions and impairs neuronal synchrony in neonatal hippocampal brain slices. In vivo, it has a minor impact on correlated spontaneous activity in the hippocampus and does not affect network activity in the intact visual cortex. Moreover, long-term effects of the developmental NKCC1 deletion on synaptic maturation, network dynamics and behavioral performance are subtle. Our data reveal a neural network function of depolarizing GABA in the hippocampus in vivo, but challenge the hypothesis that NKCC1 is essential for major aspects of hippocampal development.Competing Interest StatementThe authors have declared no competing interest.