title: Motoneuron loss associated with chronic locomotion impairments after spinal cord contusion in the rat.
abstract: Information on the nature of deficits and adaptive mechanisms occurring after spinal cord injury is essential to the design of strategies for promoting functional recovery. Motor impairments and compensations were quantified by three-dimensional kinematic analysis in freely walking rats, 6 months after mild cervical (C7) or moderate lumbar (L2) spinal cord contusion. After C7 contusion, the animals showed reduced elbow extension and wrist movement, whereas reduced knee extension was the main impairment after L2 contusion. In both cases, the duration of the walking cycle increased and forward velocity was reduced due to a longer stance phase. Histology revealed reproducible lesions extending approximately to one spinal cord segment. In the transverse plane, the lesion involved the central gray matter and adjacent axons, including the dorsal corticospinal tract, but partially spared the ventrolateral tracts. Retrograde motoneuron tracing by nerve exposure to HRP or intramuscular injection of aminostilbamidine demonstrated that C7 contusion caused the loss of approximately 40% of triceps brachii motoneurons, whereas approximately 30% of quadriceps femoris motoneurons were lost after L2 contusion. These results demonstrate permanent deficits after incomplete lesions at the spinal cord enlargements and suggest that motoneuron loss contributes to their production.
authors.affiliation: Laboratorio de Reparación Neural, Hospital Nacional de Parapléjicos, SESCAM, Toledo, Unidad Asociada al CSIC, Toledo, Spain. jcollazos@sescam.org
authors.forename: Jorge E
authors.initials: JE
authors.lastname: Collazos-Castro
authors.forename: Víctor M
authors.initials: VM
authors.lastname: Soto
authors.forename: Marcos
authors.initials: M
authors.lastname: Gutiérrez-Dávila
authors.forename: Manuel
authors.initials: M
authors.lastname: Nieto-Sampedro
mesh_terms: D000818:Animals; D001696:Biomechanical Phenomena; D016923:Cell Death / Q000502:physiology; D002574:Cervical Vertebrae; D002908:Chronic Disease; D004195:Disease Models, Animal; D005552:Forelimb / Q000294:innervation / Q000503:physiopathology; D020233:Gait Disorders, Neurologic / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D006614:Hindlimb / Q000294:innervation / Q000503:physiopathology; D008159:Lumbar Vertebrae; D008297:Male; D009046:Motor Neurons / Q000473:pathology*; D009069:Movement Disorders / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D018482:Muscle, Skeletal / Q000294:innervation / Q000503:physiopathology; D009410:Nerve Degeneration / Q000473:pathology / Q000503:physiopathology; D009434:Neural Pathways / Q000293:injuries / Q000473:pathology / Q000503:physiopathology; D010243:Paralysis / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar; D013116:Spinal Cord / Q000473:pathology* / Q000503:physiopathology; D013119:Spinal Cord Injuries / Q000473:pathology* / Q000503:physiopathology; D013997:Time Factors