During early neurodevelopment, cortical interneuron progenitors arise from the ventral telencephalic area, such as Medial Ganglionic Eminence (MGE) and Caudal Ganglionic Eminence (CGE) [1]. Secreted signaling molecules from nearby organizers, such as SHH [2,3], Wnt [4] and FGF8 [5,6], play a crucial role during this early phenotype specification of ventral telencephalon. These signals trigger the regulatory cascades that lead to cortical interneuron development by inducing key transcription factors, such as Nkx2.1 in MGE [7–9] and CoupTFII in CGE [8,9]. Once phenotypically specified in the ventral area, MGE- or CGE-derived GABAergic interneurons migrate tangentially to their target sites, where they form local synaptic connections and critically modulate cortical circuitry. MGE cells mostly mature to generate Parvalbumin+ or Somatostatin+ interneurons, which comprise more than half of the entire cortical interneuron population, while CGE cells mostly mature to generate Calretinin+ interneurons [10].
