Dysfunctional BDNF–TrkB signalling in PCs appeared to contribute to their dysfunction at an early disease stage in a mouse model of SCA6, since BDNF intensity was found to be reduced in PCs, and pre-onset treatment with a TrkB agonist improved the rotarod performance and PC firing frequency in these mice [10]. This evidence concerns the gene NTRK2 and spinocerebellar ataxia type 6.