One sentence summary: A mouse model of DYT25 dystonia, carrying a Gnal mutation disrupting striatal 13 neurotransmission, exhibits anomalous cerebello-thalamic plasticity in the non-manifesting state, but 14 theta-burst cerebellar stimulations during cholinergic-induced dystonia depress the cerebello-thalamic 15 transmission and reduce the severity of the motor symptoms. 16 17 ABSTRACT 31 Dystonia is often associated with functional alterations in the cerebello-thalamic pathways, 32 which have been proposed to contribute to the disorder by propagating pathological firing patterns to 33 the forebrain. Here, we examined the function of the cerebello-thalamic pathways in a model of DYT25 34 dystonia, mice carrying a heterozygous invalidation of Gnal gene which notably disrupts striatal 35 function, exhibiting dystonic movements and postures following systemic or striatal administration of 36 oxotremorine. Theta-burst optogenetic stimulations of the cerebellar nuclei evoked a potentiation of 37 the responses to cerebellar stimulations in the thalamus and motor cortex in WT mice, without evident 38 motor function disruption. In contrast, theta burst stimulations evoked a depression of these responses 39 only in dystonia-manifesting Gnal+/mice after oxotremorine administration, decreased the disabling 40 dystonia attacks, and increased normal active wake behaviour in Gnal+/mice. The cerebellum could 41 thus offer a gateway for a corrective treatment of motor impairments in dystonia including striatal 42 dysfunction. 43 44