Rebound burst firing activity in several cerebellar neurons arises in part from the coordinate expression of T-type calcium channel isoforms [16,17], and altered Cav3.1/α1G channel function mediated by alternative splicing may initiate abnormal burst firing leading to movement disorders, such as the ataxia and paroxysmal dyskinesia phenotypes associated with absence epilepsy in several of these mutant mouse models. This evidence concerns the gene CACNA1G and cerebellar ataxia.