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The dtsz mutant hamster represents a model of primary paroxysmal dystonia, in which stress-inducible dystonic episodes are probably related to striatal dysfunctions. In the present study, in situ hybridization was used to examine if changes of neuropeptide expression may reflect imbalances between the striatopallidal and striatonigral pathways. The analyses included the striatum and also other brain regions of dtsz hamsters in the absence of dystonia (basal) and of hamsters which exhibited severe stress-induced dystonic attacks immediately prior to sacrifice. In the striatum the basal expression of prodynorphin tended to be increased, while that of preproenkephalin tended to be decreased in mutant hamsters. In comparison to non-dystonic control hamsters, an increase in prodynorphin mRNA was restricted to the ventrolateral striatum and a decrease in both neuropeptide expression was found limbic structures (hippocampus, hypothalamus). After stressful stimulation, the neuropeptides increased in several regions in both animals groups. No changes of prodynorphin were detected in the striatum in comparison to control hamsters, but a significant decrease in preproenkephalin mRNA became evident in the anterior and dorsal striatal subregions and in nucleus accumbens during the occurrence of dystonia. Whereas previous single-unit recordings in anaesthetized mutant hamsters indicated an enhanced activity of striato-entopeduncular neurons in the absence of dystonia, changes in enkephalin expression probably reflect an abnormal activation of the striatopallidal neurons during the manifestation of dystonic attacks.