Periadolescent Maturation of GABAergic Hyperpolarization at the Axon Initial Segment

Publication date: 5 July 2017
Source:Cell Reports, Volume 20, Issue 1
Author(s): Gina Rinetti-Vargas, Khanhky Phamluong, Dorit Ron, Kevin J. Bender
Neuronal chloride levels are developmentally regulated. Early in life, high intracellular concentrations support chloride efflux and depolarization at GABAergic synapses. In mouse, intracellular chloride decreases over the first postnatal week in the somatodendritic compartment, eventually supporting mature, hyperpolarizing GABAergic inhibition. In contrast to this dendritic switch, it is less clear how GABAergic signaling at the axon initial segment (AIS) functions in mature pyramidal cells, as reports of both depolarization and hyperpolarization have been reported in the AIS past the first postnatal week. Here, we show that GABAergic signaling at the AIS of prefrontal pyramidal cells, indeed, switches polarity from depolarizing to hyperpolarizing but does so over a protracted periadolescent period. This is the most delayed maturation in chloride reversal in any structure studied to date and suggests that chandelier cells, which mediate axo-axonic inhibition, play a unique role in the periadolescent maturation of prefrontal circuits.

Graphical abstract

Teaser

Rinetti-Vargas et al. examine the development of chloride reversal potential (ECl), which determines GABAergic synapse polarity, in the axon initial segment of mouse prefrontal layer 2/3 pyramidal cells. They find that axon initial segment ECl hyperpolarizes over a periadolescent development period, eventually matching dendritic values.


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