Spinocerebellar ataxias (SCAs) are characterized by cerebellar atrophy and the degeneration of Purkinje neurons resulting from mutations in various genes. Specifically, in SCA14, the disease is caused by point mutations or deletions in the protein kinase C gamma (PKCγ) gene. PKCγ is a serine/threonine kinase predominantly expressed in cerebellar Purkinje cells, and plays a crucial role in the regulation of synapse formation and dendritic development of Purkinje cells. However, the precise mechanisms underlying these processes are not fully understood yet. In this project, our aim is to investigate the effect of PKCγ and its substrates in the development of dendritic spines of cerebellar Purkinje cells. Our approach involves utilizing PKCγ mutant mouse lines expressing a constitutively active PKCγ, resulting in an SCA14-like phenotype. These investigations are carried out using organotypic slice cultures and dissociated cerebellar cultures, followed by a morphological analysis of Purkinje cells dendritic spines. Our project addresses two critical objectives: a better understanding of the molecular network in which PKCγ is active, and gaining insights into the mechanisms responsible for cerebellar diseases and dysfunction. The ultimate goal is to identify strategies for more effective treatments correcting Purkinje cell dysfunction in cerebellar diseases.