Animals treated with reserpine, whose mechanism of action is the depletion of monoamines by the inhibition of their vesicular transporter, develop an orofacial hyperkinetic manifestation that shows similarity to both tardive dyskinesia induced by chronic treatment with haloperidol (typical antipsychotic) and changes induced by L-DOPA. Our pioneering studies have revealed that pharmacological inhibition of nitric oxide (NO) synthesis enzyme significantly decreases L-DOPA-induced dyskinesia in an experimental model of Parkinson's disease. The objective of this work is to investigate, using genetically modified animals (iNOS KO), the impact of iNOS absence in the oral involuntary movements induced by reserpine. Additionally, possible changes in the expression of activated microglia and reactive astrocytes in the reserpine model will be investigated, and if this pattern is distinct in iNOS deficient mice.
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