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 br...

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Main Authors: Antea Minetti, Elena Montagni, Nicolò Meneghetti, Francesca Macchi, Éléa Coulomb, Alessandra Martello, Alexia Tiberi, Simona Capsoni, Alberto Mazzoni, Anna Letizia Allegra Mascaro, Cristina Spalletti
Format: Article
Language:English
Published: Nature Portfolio 2025-07-01
Series:npj Parkinson's Disease
Online Access:https://doi.org/10.1038/s41531-025-01052-6
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author Antea Minetti
Elena Montagni
Nicolò Meneghetti
Francesca Macchi
Éléa Coulomb
Alessandra Martello
Alexia Tiberi
Simona Capsoni
Alberto Mazzoni
Anna Letizia Allegra Mascaro
Cristina Spalletti
author_facet Antea Minetti
Elena Montagni
Nicolò Meneghetti
Francesca Macchi
Éléa Coulomb
Alessandra Martello
Alexia Tiberi
Simona Capsoni
Alberto Mazzoni
Anna Letizia Allegra Mascaro
Cristina Spalletti
author_sort Antea Minetti
collection DOAJ
description 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 motor cortex. Synaptic imbalances and microglial activation further point to a multifaceted cortical response to dopaminergic degeneration, revealing inhibitory dysfunction, oscillatory instability, structural remodeling, and neuroinflammation. Our results link PD to cortical instability and highlight cortical plasticity as a promising target for therapeutic intervention.
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institution Kabale University
issn 2373-8057
language English
publishDate 2025-07-01
publisher Nature Portfolio
record_format Article
series npj Parkinson's Disease
spelling doaj-art-d72a1a82df5d4b9dbcf409e67d79a1312025-08-20T03:37:23ZengNature Portfolionpj Parkinson's Disease2373-80572025-07-0111112110.1038/s41531-025-01052-6Parkinsonism disrupts cortical function by dysregulating oscillatory, network and synaptic activity of parvalbumin positive interneuronsAntea Minetti0Elena Montagni1Nicolò Meneghetti2Francesca Macchi3Éléa Coulomb4Alessandra Martello5Alexia Tiberi6Simona Capsoni7Alberto Mazzoni8Anna Letizia Allegra Mascaro9Cristina Spalletti10Neuroscience Institute, National Research Council (CNR)Neuroscience Institute, National Research Council (CNR)The Biorobotics Institute, Scuola Superiore Sant’Anna (SSSA)Neuroscience Institute, National Research Council (CNR)Neuroscience Institute, National Research Council (CNR)Neuroscience Institute, National Research Council (CNR)Neuroscience Institute, National Research Council (CNR)Section of Human Physiology, Department of Neuroscience and Rehabilitation, University of FerraraThe Biorobotics Institute, Scuola Superiore Sant’Anna (SSSA)Neuroscience Institute, National Research Council (CNR)Neuroscience Institute, National Research Council (CNR)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 motor cortex. Synaptic imbalances and microglial activation further point to a multifaceted cortical response to dopaminergic degeneration, revealing inhibitory dysfunction, oscillatory instability, structural remodeling, and neuroinflammation. Our results link PD to cortical instability and highlight cortical plasticity as a promising target for therapeutic intervention.https://doi.org/10.1038/s41531-025-01052-6
spellingShingle Antea Minetti
Elena Montagni
Nicolò Meneghetti
Francesca Macchi
Éléa Coulomb
Alessandra Martello
Alexia Tiberi
Simona Capsoni
Alberto Mazzoni
Anna Letizia Allegra Mascaro
Cristina Spalletti
Parkinsonism disrupts cortical function by dysregulating oscillatory, network and synaptic activity of parvalbumin positive interneurons
npj Parkinson's Disease
title Parkinsonism disrupts cortical function by dysregulating oscillatory, network and synaptic activity of parvalbumin positive interneurons
title_full Parkinsonism disrupts cortical function by dysregulating oscillatory, network and synaptic activity of parvalbumin positive interneurons
title_fullStr Parkinsonism disrupts cortical function by dysregulating oscillatory, network and synaptic activity of parvalbumin positive interneurons
title_full_unstemmed Parkinsonism disrupts cortical function by dysregulating oscillatory, network and synaptic activity of parvalbumin positive interneurons
title_short Parkinsonism disrupts cortical function by dysregulating oscillatory, network and synaptic activity of parvalbumin positive interneurons
title_sort parkinsonism disrupts cortical function by dysregulating oscillatory network and synaptic activity of parvalbumin positive interneurons
url https://doi.org/10.1038/s41531-025-01052-6
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