Exercise decreases aberrant corticostriatal plasticity in an animal model of l-DOPA-induced dyskinesia.

Autor:	Speck AE; Experimental Laboratory of Neurodegenerative Disease, Department of Pharmacology, Center of Biological Sciences, Federal University of Santa Catarina (UFSC), Florianópolis, Brazil.; CNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal., Aguiar AS Jr; CNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.; Biology of Exercise Lab, Department of Health Sciences, Federal University of Santa Catarina (UFSC), Araranguá, Brazil., Ferreira SG; CNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal., Silva HB; CNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal., Tomé ÂR; CNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal., Agostinho P; CNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.; Faculty of Medicine, University of Coimbra, Coimbra, Portugal., Cunha RA; CNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.; Faculty of Medicine, University of Coimbra, Coimbra, Portugal., Prediger RD; Experimental Laboratory of Neurodegenerative Disease, Department of Pharmacology, Center of Biological Sciences, Federal University of Santa Catarina (UFSC), Florianópolis, Brazil.
Jazyk:	angličtina
Zdroj:	American journal of physiology. Regulatory, integrative and comparative physiology [Am J Physiol Regul Integr Comp Physiol] 2021 Apr 01; Vol. 320 (4), pp. R541-R546. Date of Electronic Publication: 2021 Feb 03.
DOI:	10.1152/ajpregu.00295.2020
Abstrakt:	Physical exercise attenuates the development of l-3,4-dihydroxyphenylalanine (l-DOPA)-induced dyskinesia (LID) in 6-hydroxydopamine-induced hemiparkinsonian mice through unknown mechanisms. We now tested if exercise normalizes the aberrant corticostriatal neuroplasticity associated with experimental murine models of LID. C57BL/6 mice received two unilateral intrastriatal injections of 6-hydroxydopamine (12 μg) and were treated after 3 wk with l-DOPA/benserazide (25/12.5 mg/kg) for 4 wk, with individualized moderate-intensity running (60%-70% V̇o 2peak ) or not (untrained). l-DOPA converted the pattern of plasticity in corticostriatal synapses from a long-term depression (LTD) into a long-term potentiation (LTP). Exercise reduced LID severity and decreased aberrant LTP. These results suggest that exercise attenuates abnormal corticostriatal plasticity to decrease LID.
Databáze:	MEDLINE
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