Parkinsonism disrupts cortical function by dysregulating oscillatory, network and synaptic activity of parvalbumin positive interneurons.

ABSTRACT: Identifying novel and accessible therapeutic targets for Parkinson's Disease (PD) remains a pressing goal. Growing evidence implicates cortical dysfunctions in PD-related symptoms, yet the mechanisms-especially those involving parvalbumin-positive interneurons (PV-INs), key regulators of brain oscillations and plasticity-are not fully understood. In this study, we investigate how PD alters PV-IN network and cortical oscillatory dynamics using the 6-hydroxydopamine (6-OHDA) mouse model. Through an integrated approach combining electrophysiological recordings, wide-field calcium imaging, and histological analysis, we reveal a profound cascade of cortical changes. These include pathological hyperactivity above 100 Hz during movement and severe disruptions in PV-IN connectivity across the moto

SUBMITTER: Minetti A 

PROVIDER: S-EPMC12215278 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature