Developmental localization of potassium chloride co-transporter 2 (KCC2), GABA and vesicular GABA transporter (VGAT) in the postnatal mouse somatosensory cortex

Gamma-amino butyric acid (GABA) mediates the hyperpolarization of membrane potential, negatively regulating glutamatergic activity in the adult brain, whereas, mediates depolarization in the immature brain. This developmental shift in GABA actions is induced by the expression of potassium chloride cotransporter 2 (KCC2). In this study, we focused on the developing mouse somatosensory cortex, where the barrel structure in layer 4 is altered by the whisker-lesion during the critical period, before postnatal day 4 (P4). First, to clarify the time-course of postnatal changes in GABA actions, we investigated the developmental localization of KCC2. Second, to reveal its spatial and temporal relationship with GABA synapse formation, we examined the developmental localization of GABA and vesicular GABA transporter. KCC2 was localized within the pyramidal cells in layer 5 after P3, granule cells in layer 4 after P5 and neurons in layers 2 and 3 after P7, indicating that KCC2 was expressed in the chronological order of neuronal settling at the destination. The onset of KCC2 localization was almost concomitant with the formation of GABA synapses, suggesting that GABA was inhibitory after GABA synapse formation. Furthermore, extrasynaptically released GABA might be involved in the maintenance of activity-dependent plasticity as an excitatory transmitter during the critical period