The role of neuronal chloride levels in postnatal development of inhibitory synapses
GABA currents shift from depolarizing to hyperpolarizing because intracellular chloride levels decrease during postnatal development. The GABA shift is mistimed in patients and mouse models for neurodevelopmental disorders. It is currently unclear whether a mistimed GABA shift is cause or consequence for alterations in synaptic transmission in these mouse models. Here, we assess the consequences of mistimed GABA shift on inhibitory transmission in hippocampal slice cultures. Our results indicate that neuronal chloride levels play a complex role in postnatal development of inhibitory synapses.
