Veröffentlichung in PNAS

Significance

Neuronal circuits develop in an activity-dependent manner. In vitro data suggest that the intracellular accumulation of chloride—a universal characteristic of immature nerve cells—drives network maturation through a depolarizing action of the neurotransmitter GABA. We here demonstrate that deletion of the chloride cotransporter NKCC1 from forebrain pyramidal cells severely impairs hippocampal network synchrony in vitro. In contrast, NKCC1 has weak and event type-dependent effects on spontaneous network activity in vivo, and loss of NKCC1 leaves the maturation of synaptic properties, network dynamics, and hippocampus-dependent behaviors largely unaffected. Our data reveal a subtle neural network function of NKCC1 in hippocampal glutamatergic neurons in vivo, but challenge the assertion that NKCC1 in this major cell type is central to hippocampal development.