neurons compared to control cells (Fig. 3b; Extended Data Fig. 9h, i), similar to what we have previously shown in TS hiPSC-derived glutamatergic neurons26. We investigated the migration of Dlxi1/2b::eGFP+ cells in fused hSS-hCS (Fig. 3c; Extended Data Fig. 9j; Supplementary Video 7) and found an increase in saltation frequency in neurons from all three TS patients (Fig. 3d; Extended Data Fig. 9k) in agreement with the role of calcium in interneuron motility17. Interestingly, the saltation length and the speed when mobile were reduced in TS (Fig. 3d, e; Extended Data Fig. 9l, m) resulting in a less efficient migration (Fig. 3f). Moreover, this effect was cell-autonomous because migration of Dlxi1/2b::eGFP+ cells from TS-hSS into control-hCS did not influence the phenotype (Fig. 3d, e; Extended Data Fig. 9k–m). To further validate these results, we electroporated cDNA encoding TS– and wild type (WT)– CaV1.2 into slices of mouse E14 ganglionic eminences and performed live imaging (Extended Data Fig. 9n, o). We observed a defect in mouse TS-CaV1.2 electroporated neurons displaying more frequent but shorter saltations (Extended Data Fig. 9p, q). To determine if the TS migratory phenotype was a result of LTCCs activity and could be reversed, we treated fused hSS-hCS
