Neurogenesis and interneuron integration are crucial for maintaining cortical circuit functionality. In the medial ganglionic eminences (MGE), ventral radial glia (vRG) predominantly generates somatostatin-expressing (SST+) interneurons through direct neurogenesis in the neocortex. However, the mechanism guiding vRG to asymmetrically divide and produce either SST+ interneuron or intermediate progenitor (IP) remains unclear. This study identifies a novel subpopulation of vRG, characterized by the expression of Anoctamin 1/TMEM16a (ANO1), a Ca2+-activated Cl− channel predominantly found in Fabp7+/Sox2+ vRGs. ANO1 deficiency significantly reduces vRG proliferation, disrupting the ratio of SST+ interneuron to IP, and correlates with changes in the number of parvalbumin-expressing interneurons. Electrophysiological recordings from E12.5 brain slices reveal that ANO1 modulates GABA-dependent Ca2+ influx via Orai1. This regulation is essential for directing the production of SST+ interneuron or IP during mouse forebrain development. Our findings provide novel insights into the Ca2+ regulatory mechanisms mediated by ion channels, underlying early neural development.