Primary dystonia is a common movement disorder with an unknown pathophysiology, but basal ganglia dysfunctions seem to play a critical role. Previous studies in the dtsz mutant hamster, an animal model of primary paroxysmal dystonia, demonstrated a deficit of striatal gamma-amino-butyric acid (GABA) containing interneurons, which normalized at the age of the spontaneous remission of the symptoms. Whereas the reduction of striatal parvalbumin-reactive interneurons is thought to be critically involved in the pathogenesis of dystonia in the hamster mutant, the impact of a reduced density of nitric oxide synthase (NOS) reactive interneurons within the striatum is still unclear. Beside GABA, these interneurons contain somatostatin, neuropeptide Y, nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) and neuronal NOS, an enzyme which produces NO after the activation of the interneurons. In order to clarify if the reduced density of NOS-reactive interneurons contributes by an altered striatal production of nitric oxide (NO) to the occurrence of dystonic attacks in the hamster mutant, we performed microinjections of the NOS inhibitors 7-nitroindazole (7-NI) and Nomega-propyl-L-arginine (NPLA) and of the precursor of NO, L-arginine, into the striata of dtsz hamsters. Neither 7-NI (0.1 and 0.4 microg per hemisphere) and NPLA (2.5, 5 and 7.5 microg per hemisphere) nor L-arginine (9 and 18 microg per hemisphere) exerted any effects on the severity of dystonic movements in the dtsz mutant. Therefore, a critical involvement of striatal changes of NO in the pathophysiology of dystonic attacks in the dtsz hamster cannot be confirmed by the results of these pharmacological examinations. In view of the ontogenetic reduction of the other types of GABAergic interneurons, the deficit of NOS-reactive interneurons is possibly due to the same underlying unknown mechanism, but is less important for the pathophysiology of primary paroxysmal dystonia in the dtsz hamster mutant.