Immune control of the basal ganglia network: Interleukin-17 as a key modulator of striatal synaptic plasticity

The basal ganglia (BG) network exerts a key role in the integration of cortical inputs and is fundamental to motor learning, behavior, emotional responses, and cognitive functions. Little is known about how immune cells and soluble immune mediators influence BG activity. Interleukin-17A (IL-17A) is...

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Main Authors: Andrea Mancini, Laura Bellingacci, Jacopo Canonichesi, Miriam Sciaccaluga, Alfredo Megaro, Elisa Zianni, Maria De Carluccio, Marilena Pariano, Edoardo Emiliano, Alessandro Tozzi, Cinzia Costa, Teresa Zelante, Luigina Romani, Maria Teresa Viscomi, Fabrizio Gardoni, Paolo Calabresi, Lucilla Parnetti, Massimiliano Di Filippo
Format: Article
Language:English
Published: Elsevier 2025-09-01
Series:Neurobiology of Disease
Online Access:http://www.sciencedirect.com/science/article/pii/S0969996125002104
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author Andrea Mancini
Laura Bellingacci
Jacopo Canonichesi
Miriam Sciaccaluga
Alfredo Megaro
Elisa Zianni
Maria De Carluccio
Marilena Pariano
Edoardo Emiliano
Alessandro Tozzi
Cinzia Costa
Teresa Zelante
Luigina Romani
Maria Teresa Viscomi
Fabrizio Gardoni
Paolo Calabresi
Lucilla Parnetti
Massimiliano Di Filippo
author_facet Andrea Mancini
Laura Bellingacci
Jacopo Canonichesi
Miriam Sciaccaluga
Alfredo Megaro
Elisa Zianni
Maria De Carluccio
Marilena Pariano
Edoardo Emiliano
Alessandro Tozzi
Cinzia Costa
Teresa Zelante
Luigina Romani
Maria Teresa Viscomi
Fabrizio Gardoni
Paolo Calabresi
Lucilla Parnetti
Massimiliano Di Filippo
author_sort Andrea Mancini
collection DOAJ
description The basal ganglia (BG) network exerts a key role in the integration of cortical inputs and is fundamental to motor learning, behavior, emotional responses, and cognitive functions. Little is known about how immune cells and soluble immune mediators influence BG activity. Interleukin-17A (IL-17A) is in the spotlight for its emerging role as a neuromodulator of cortical synaptic transmission and plasticity in physiological and pathological conditions. However, its role at the level of subcortical structures such as the BG circuit is still unclear. In this study, we demonstrate that striatal medium spiny neurons (MSNs) highly express IL-17RA and that the IL-17 axis contributes to the physiological expression of synaptic plasticity in these cells. Indeed, long-term potentiation (LTP) induction was significantly reduced in mice lacking IL-17A or IL-17RA. This effect might rely on an altered glutamatergic transmission, as synaptic expression of NMDAR subunit GluN2B is reduced in mice lacking IL-17A. At the same time, exposure to high concentrations of IL-17A was found to impair LTP induction through modulation of NMDAR currents. These results suggest a dual effect of this cytokine on striatal synaptic plasticity, showing the IL-17 axis as a key neuromodulator of the BG circuit, with potential implications in the pathogenesis of neuroinflammatory and neuropsychiatric disorders.
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spelling doaj-art-ae42cfd754ec4a6aa4b9e8df4a2c4bb92025-08-20T03:55:48ZengElsevierNeurobiology of Disease1095-953X2025-09-0121310699410.1016/j.nbd.2025.106994Immune control of the basal ganglia network: Interleukin-17 as a key modulator of striatal synaptic plasticityAndrea Mancini0Laura Bellingacci1Jacopo Canonichesi2Miriam Sciaccaluga3Alfredo Megaro4Elisa Zianni5Maria De Carluccio6Marilena Pariano7Edoardo Emiliano8Alessandro Tozzi9Cinzia Costa10Teresa Zelante11Luigina Romani12Maria Teresa Viscomi13Fabrizio Gardoni14Paolo Calabresi15Lucilla Parnetti16Massimiliano Di Filippo17Section of Neurology and Laboratory of Experimental Neurology, Department of Medicine and Surgery, University of Perugia, Perugia, ItalySection of Physiology and Biochemistry, Department of Medicine and Surgery, University of Perugia, Perugia, ItalySection of Neurology and Laboratory of Experimental Neurology, Department of Medicine and Surgery, University of Perugia, Perugia, ItalySection of Neurology and Laboratory of Experimental Neurology, Department of Medicine and Surgery, University of Perugia, Perugia, ItalySection of Neurology and Laboratory of Experimental Neurology, Department of Medicine and Surgery, University of Perugia, Perugia, ItalyDepartment of Pharmacological and Biomolecular Sciences, University of Milan, 20133 Milan, ItalyDepartment of Neuroscience and Neurorehabilitation, IRCCS San Raffaele, Rome, italy; Department of Neuroscience, Università Cattolica del Sacro Cuore, Rome, ItalySection of Neurophysiopathology, “S.M. della Misericordia” Hospital, Perugia, ItalySection of Neurology and Laboratory of Experimental Neurology, Department of Medicine and Surgery, University of Perugia, Perugia, ItalySection of Physiology and Biochemistry, Department of Medicine and Surgery, University of Perugia, Perugia, ItalySection of Neurology and Laboratory of Experimental Neurology, Department of Medicine and Surgery, University of Perugia, Perugia, Italy; Section of Neurophysiopathology, “S.M. della Misericordia” Hospital, Perugia, ItalySection of Pathology, Department of Medicine and Surgery, University of Perugia, Perugia, ItalySection of Pathology, Department of Medicine and Surgery, University of Perugia, Perugia, ItalySection of Histology and Embryology, Department of Life Science and Public Health, Università Cattolica del Sacro Cuore, Rome, Italy; Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, ItalyDepartment of Pharmacological and Biomolecular Sciences, University of Milan, 20133 Milan, ItalyDepartment of Neuroscience, Università Cattolica del Sacro Cuore, Rome, Italy; Section of Neurology, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, ItalySection of Neurology and Laboratory of Experimental Neurology, Department of Medicine and Surgery, University of Perugia, Perugia, ItalySection of Neurology and Laboratory of Experimental Neurology, Department of Medicine and Surgery, University of Perugia, Perugia, Italy; Corresponding author at: Section of Neurology, Dept. of Medicine and Surgery, University of Perugia, Italy.The basal ganglia (BG) network exerts a key role in the integration of cortical inputs and is fundamental to motor learning, behavior, emotional responses, and cognitive functions. Little is known about how immune cells and soluble immune mediators influence BG activity. Interleukin-17A (IL-17A) is in the spotlight for its emerging role as a neuromodulator of cortical synaptic transmission and plasticity in physiological and pathological conditions. However, its role at the level of subcortical structures such as the BG circuit is still unclear. In this study, we demonstrate that striatal medium spiny neurons (MSNs) highly express IL-17RA and that the IL-17 axis contributes to the physiological expression of synaptic plasticity in these cells. Indeed, long-term potentiation (LTP) induction was significantly reduced in mice lacking IL-17A or IL-17RA. This effect might rely on an altered glutamatergic transmission, as synaptic expression of NMDAR subunit GluN2B is reduced in mice lacking IL-17A. At the same time, exposure to high concentrations of IL-17A was found to impair LTP induction through modulation of NMDAR currents. These results suggest a dual effect of this cytokine on striatal synaptic plasticity, showing the IL-17 axis as a key neuromodulator of the BG circuit, with potential implications in the pathogenesis of neuroinflammatory and neuropsychiatric disorders.http://www.sciencedirect.com/science/article/pii/S0969996125002104
spellingShingle Andrea Mancini
Laura Bellingacci
Jacopo Canonichesi
Miriam Sciaccaluga
Alfredo Megaro
Elisa Zianni
Maria De Carluccio
Marilena Pariano
Edoardo Emiliano
Alessandro Tozzi
Cinzia Costa
Teresa Zelante
Luigina Romani
Maria Teresa Viscomi
Fabrizio Gardoni
Paolo Calabresi
Lucilla Parnetti
Massimiliano Di Filippo
Immune control of the basal ganglia network: Interleukin-17 as a key modulator of striatal synaptic plasticity
Neurobiology of Disease
title Immune control of the basal ganglia network: Interleukin-17 as a key modulator of striatal synaptic plasticity
title_full Immune control of the basal ganglia network: Interleukin-17 as a key modulator of striatal synaptic plasticity
title_fullStr Immune control of the basal ganglia network: Interleukin-17 as a key modulator of striatal synaptic plasticity
title_full_unstemmed Immune control of the basal ganglia network: Interleukin-17 as a key modulator of striatal synaptic plasticity
title_short Immune control of the basal ganglia network: Interleukin-17 as a key modulator of striatal synaptic plasticity
title_sort immune control of the basal ganglia network interleukin 17 as a key modulator of striatal synaptic plasticity
url http://www.sciencedirect.com/science/article/pii/S0969996125002104
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