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 with LTCCs blockers (Fig. 3g; Extended Data Fig. 9r–u). We found that application of the LTCCs blocker nimodipine significantly reduced saltation length and speed when mobile in control Dlxi1/2b::eGFP+ cells. However, the deficit in these parameters was rescued in TS Dlxi1/2b::eGFP+ cells following exposure to nimodipine. Moreover, roscovitine, a cyclin-dependent kinase inhibitor that increases voltage-dependent inactivation of CaV1.227,28, also rescued saltation length in TS Dlxi1/2b::eGFP+ cells. These results indicate that the migration defect in interneurons carrying the TS gain-of-function mutation can be restored by reducing the activity of LTCCs.
