Dystonias are movement disorders whose pathomechanism is largely unknown. Dystonic dtsz hamsters represent a model of primary dystonias, where alterations of striatal interneuron density and long-term potentiation (LTP) were described. In the current work, using cortico-striatal slices, we explore whether long-term potentiation and long-term depression (LTD) are altered in dtsz hamsters. Field extracellular recordings were conducted in dorsomedial striatum, and white matter was stimulated. Short and long-term plasticity as well as input-output relationships were analysed. In dtsz , field responses and LTP were enhanced in dystonic hamsters. LTD was absent in dystonic hamsters compared to the control. Paired-pulse facilitation showed no alterations. In summary, the study shows that a change in long term plasticity is involved in the manifestation of paroxysmal dystonia in the dtsz mutant.