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GABA emerges as a trophic signal during rat neocortical development in which it modulates proliferation of neuronal progenitors in the ventricular/subventricular zone (VZ/SVZ) and mediates radial migration of neurons from the VZ/SVZ to the cortical plate/subplate (CP/SP) region. In this study we investigated the role of GABA in the earliest phases of neuronal differentiation in the CP/SP. GABAergic-signaling components emerging during neuronal lineage progression were comprehensively characterized using flow cytometry and immunophenotyping together with physiological indicator dyes. During migration from the VZ/SVZ to the CP/SP, differentiating cortical neurons became predominantly GABAergic, and their dominant GABAA receptor subunit expression pattern changed from α4β1γ1 to α3β3γ2γ3 coincident with an increasing potency of GABA on GABAA receptor-mediated depolarization. GABAA autoreceptor/Cl− channel activity in cultured CP/SP neurons dominated their baseline potential and indirectly their cytosolic Ca2+(Ca2+c) levels via Ca2+ entry through L-type Ca2+channels. Block of this autocrine circuit at the level of GABA synthesis, GABAA receptor activation, intracellular Cl− ion homeostasis, or L-type Ca2+ channels attenuated neurite outgrowth in most GABAergic CP/SP neurons. In the absence of autocrine GABAergic signaling, neuritogenesis could be preserved by depolarizing cells and elevating Ca2+c. These results reveal a morphogenic role for GABA during embryonic neocortical neuron development that involves GABAA autoreceptors and L-type Ca2+ channels.

the journal of neuroscience/the journal of neuroscience

GABA Expression Dominates Neuronal Lineage Progression in the Embryonic Rat Neocortex and Facilitates Neurite Outgrowth via GABA<sub>A</sub>Autoreceptor/Cl<sup>−</sup>Channels

GABA Expression Dominates Neuronal Lineage Progression in the Embryonic Rat Neocortex and Facilitates Neurite Outgrowth via GABAAAutoreceptor/Cl−Channels

GABA Expression Dominates Neuronal Lineage Progression in the Embryonic Rat Neocortex and Facilitates Neurite Outgrowth via GABA_AAutoreceptor/Cl⁻Channels