KCND2 and Huntington disease: In iSPNs from both BACHD and Q175 HD mice, the ratio of distal to proximal bAP-evoked Ca2+ transients were smaller than in age-matched, wild-type iSPNs; this deficit was corrected by knocking down the expression of Kv4.2 subunits or by pharmacologically inhibiting Kv4 channels with 4-AP.