title: Electrical stimulation impairs early functional recovery and accentuates skeletal muscle atrophy after sciatic nerve crush injury in rats.
abstract: Neuromuscular recovery after peripheral nerve lesion depends on the regeneration of severed axons that re-establish their functional connection with the denervated muscle. The aim of this study was to determine the effects of electrical stimulation (ES) on the neuromuscular recovery after nerve crush injury in rats. Electrical stimulation was carried out on the tibialis anterior (TA) muscle after sciatic nerve crush injury in a rat model. Six ES sessions were administered every other day starting from day 3 postinjury until the end of the experiment (day 14). The sciatic functional index was calculated. Muscle excitability, neural cell adhesion molecule (N-CAM) expression, and muscle fiber cross-sectional area (CSA) were accessed from TA muscle. Regenerated sciatic nerves were analyzed by light and confocal microscopy. Both treated (crush+ES) and untreated (crush) groups had their muscle weight and CSA decreased compared with the normal group (P < 0.05). Electrical stimulation accentuated muscle fiber atrophy more in the crush+ES than in the crush group (P < 0.05). N-CAM expression increased in both crush and crush+ES groups compared with the normal group (P < 0.05). Regenerated nerves revealed no difference between the crush and crush+ES groups. Nevertheless, functional recovery at day 14 post-injury was significantly lower in crush+ES group compared with the crush group. In addition, the crush+ES group had chronaxie values significantly higher on days 7 and 13 compared with the crush group, which indicates a decrease in muscle excitability in the crush+ES animals. The results of this study do not support a benefit of the tested protocol of ES during the period of motor nerve recovery following injury.
authors.affiliation: Unit of Thermophototherapy, Department of Physical Therapy, Federal University of São Carlos, Rodovia Washington Luis, Km 235, CP 676, CEP 13.565-905, São Carlos, SP, Brazil.
authors.forename: Davilene
authors.initials: D
authors.lastname: Gigo-Benato
authors.forename: Thiago Luiz
authors.initials: TL
authors.lastname: Russo
authors.forename: Stefano
authors.initials: S
authors.lastname: Geuna
authors.forename: Natalia Rezende Santa Rosa
authors.initials: NR
authors.lastname: Domingues
authors.forename: Tania Fátima
authors.initials: TF
authors.lastname: Salvini
authors.forename: Nivaldo Antonio
authors.initials: NA
authors.lastname: Parizotto
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D004195:Disease Models, Animal; D004599:Electric Stimulation Therapy / Q000009:adverse effects* / Q000379:methods; D008297:Male; D008564:Membrane Potentials / Q000502:physiology; D009119:Muscle Contraction / Q000502:physiology; D009121:Muscle Denervation / Q000009:adverse effects; D018485:Muscle Fibers, Skeletal / Q000378:metabolism / Q000473:pathology; D018482:Muscle, Skeletal / Q000294:innervation / Q000473:pathology / Q000503:physiopathology*; D009133:Muscular Atrophy / Q000473:pathology / Q000503:physiopathology*; D019006:Neural Cell Adhesion Molecules / Q000378:metabolism; D009431:Neural Conduction / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D020127:Recovery of Function / Q000502:physiology*; D020426:Sciatic Neuropathy / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy*; D013997:Time Factors
chemical_list: D015415:Biomarkers; D019006:Neural Cell Adhesion Molecules