Parkinson's disease is a prevalent neurodegenerative disorder characterized by motor impairments including rigidity, bradykinesia and tremor. L-3,4-dihydroxyphenylalanine (L-DOPA) keeps being the standard treatment for Parkinson's disease. But long-term treatment often leads to L-DOPA induced dyskinesias (LIDs): abnormal involuntary movements (AIMs) that significantly impact patients' quality of life. Drugs acting on nicotinic acetylcholine receptors (nAChRs) have emerged as a potential treatment for managing LIDs, since nicotine, shows promise in alleviating LIDs in animal models. Positive allosteric modulators acting via nAChRs of classes α4β2 and α7, such as NS9283 and PNU120596, respectively, have demonstrated therapeutic benefits in preclinical studies using parkinsonian models. Here we investigate the actions of both NS9283 and PNU120596 acting independently or enhancing nicotine's therapeutic effects on LIDs, seeking for novel therapeutic strategies for LIDs management. We used both behavioral assessments and an in vitro pharmacological bioassay previously reported to evaluate striatal microcircuit activity at the histological level in brain slices of dyskinetic mice. Our results show that PNU120596 administered alone is a potent anti-dyskinetic drug, its action not being improved by the presence of nicotine. In contrast, NS9283 has no action administered alone and does not significantly improve nicotine actions. Behavioral results coincide with the in vitro bioassay using principal components analysis of calcium imaging activity: PNU120596 actions in the striatal microcircuit clearly reduce and change active neurons in agreement with dyskinesia reduction. These findings point towards striatal α7-nAChRs positive allosteric modulators as potentially novel adjuvant drugs to manage LIDs.