NKCC-1 mediated Cl uptake in immature CA3 pyramidal neurons is sufficient to compensate phasic GABAergic inputs.

Activation of GABA receptors causes in immature neurons a functionally relevant decrease in the intracellular Cl concentration ([Cl]), a process termed ionic plasticity. Amount and duration of ionic plasticity depends on kinetic properties of [Cl] homeostasis. In order to characterize the capacity of Cl accumulation and to quantify the effect of persistent GABAergic activity on [Cl], we performed gramicidin-perforated patch-clamp recordings from CA3 pyramidal neurons of immature (postnatal day 4-7) rat hippocampal slices.

Spines slow down dendritic chloride diffusion and affect short-term ionic plasticity of GABAergic inhibition.

Cl(-) plays a crucial role in neuronal function and synaptic inhibition. However, the impact of neuronal morphology on the diffusion and redistribution of intracellular Cl(-) is not well understood. The role of spines in Cl(-) diffusion along dendritic trees has not been addressed so far.