title: Peripheral and central changes combine to induce motor behavioral deficits in a moderate repetition task.
abstract: Repetitive motion disorders, such as carpal tunnel syndrome and focal hand dystonia, can be associated with tasks that require prolonged, repetitive behaviors. Previous studies using animal models of repetitive motion have correlated cortical neuroplastic changes or peripheral tissue inflammation with fine motor performance. However, the possibility that both peripheral and central mechanisms coexist with altered motor performance has not been studied. In this study, we investigated the relationship between motor behavior changes associated with repetitive behaviors and both peripheral tissue inflammation and cortical neuroplasticity. A rat model of reaching and grasping involving moderate repetitive reaching with negligible force (MRNF) was used. Rats performed the MRNF task for 2 h/day, 3 days/week for 8 weeks. Reach performance was monitored by measuring reach rate/success, daily exposure, reach movement reversals/patterns, reach/grasp phase times, grip strength and grooming function. With cumulative task exposure, reach performance, grip strength and agility declined while an inefficient food retrieval pattern increased. In S1 of MRNF rats, a dramatic disorganization of the topographic forepaw representation was observed, including the emergence of large receptive fields located on both the wrist/forearm and forepaw with alterations of neuronal properties. In M1, there was a drastic enlargement of the overall forepaw map area, and of the cortex devoted to digit, arm-digits and elbow-wrist responses. In addition, unusually low current amplitude evoked digit movements. IL-1 beta and TNF-alpha increased in forearm flexor muscles and tendons of MRNF animals. The increases in IL-1 beta and TNF-alpha negatively correlated with grip strength and amount of current needed to evoke forelimb movements. This study provides strong evidence that both peripheral inflammation and cortical neuroplasticity jointly contribute to the development of chronic repetitive motion disorders.
authors.affiliation: UMR 6149 Neurobiologie Intégrative et Adaptative, CNRS-Aix-Marseille Université, Pôle 3C, Case B, 3 Place Victor Hugo, 13331, Marseille Cedex 03, France.
authors.forename: Jacques-Olivier
authors.initials: JO
authors.lastname: Coq
authors.forename: Ann E
authors.initials: AE
authors.lastname: Barr
authors.forename: Fabrizio
authors.initials: F
authors.lastname: Strata
authors.forename: Michael
authors.initials: M
authors.lastname: Russier
authors.forename: David M
authors.initials: DM
authors.lastname: Kietrys
authors.forename: Michael M
authors.initials: MM
authors.lastname: Merzenich
authors.forename: Nancy N
authors.initials: NN
authors.lastname: Byl
authors.forename: Mary F
authors.initials: MF
authors.lastname: Barbe
mesh_terms: D000818:Animals; D001522:Behavior, Animal / Q000502:physiology*; D001931:Brain Mapping; D002490:Central Nervous System / Q000378:metabolism / Q000473:pathology*; D012090:Cumulative Trauma Disorders / Q000378:metabolism / Q000473:pathology*; D016207:Cytokines / Q000378:metabolism; D004594:Electrophysiology; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005552:Forelimb / Q000502:physiology; D018737:Hand Strength / Q000502:physiology; D007249:Inflammation / Q000473:pathology; D009044:Motor Cortex / Q000503:physiopathology; D017933:Peripheral Nervous System / Q000378:metabolism / Q000473:pathology*; D011597:Psychomotor Performance / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013003:Somatosensory Cortex / Q000503:physiopathology; D013710:Tendons / Q000378:metabolism
chemical_list: D016207:Cytokines
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