title: Better functional outcome of compression spinal cord injury in mice is associated with enhanced H-reflex responses.
abstract: Alterations in spinal reflexes and functional improvements occur after incomplete spinal cord injury but the relationship between these phenomena is not understood. Here we show that spontaneous functional recovery after compression injury of the spinal cord at low-thoracic level (Th10-12) in C57BL/6J mice is associated with a progressively increasing, over 3 months, excitability of the plantar H-reflex. The stimulation rate-sensitive H-reflex depression, already strongly reduced at 1 week after injury, when compared with non-injured mice, decreased further during the observation time period. Twelve weeks after injury, the degree of motor recovery estimated by single-frame motion analysis in individual animals correlated positively with their H-reflex responses at 2-Hz stimulation. Functional recovery and reflex alterations were accompanied by an increase in glycine/GABAergic and glutamatergic terminals around motoneuron cell bodies between 6 and 12 weeks after injury. Enhanced H-reflex responses at frequencies between 0.1 and 5 Hz were also observed in mice deficient in the extracellular matrix glycoprotein tenascin-R and the adhesion molecule close homolog of L1, mice previously shown to have better motor recovery after spinal cord injury than wild-type littermates. These results indicate that better functional outcome of compression spinal cord injury in mice is associated with alterations of the monosynaptic reflex pathway which facilitate motoneuron recruitment. Our observations support the view that plasticity of spinal circuitries underlies specific aspects of motor recovery and demonstrate the usefulness of H-reflex analyses in studies on spinal cord injury in mice.
authors.affiliation: Zentrum für Molekulare Neurobiologie, Universität Hamburg, Martinistrasse 52, D-20246 Hamburg, Germany.
authors.forename: Hyun Joon
authors.initials: HJ
authors.lastname: Lee
authors.forename: Igor
authors.initials: I
authors.lastname: Jakovcevski
authors.forename: Nevena
authors.initials: N
authors.lastname: Radonjic
authors.forename: Laura
authors.initials: L
authors.lastname: Hoelters
authors.forename: Melitta
authors.initials: M
authors.lastname: Schachner
authors.forename: Andrey
authors.initials: A
authors.lastname: Irintchev
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001703:Biophysics; D015815:Cell Adhesion Molecules / Q000172:deficiency; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D004195:Disease Models, Animal; D004558:Electric Stimulation / Q000379:methods; D005260:Female; D005998:Glycine / Q000378:metabolism; D006181:H-Reflex / Q000235:genetics / Q000502:physiology*; D008124:Locomotion / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009046:Motor Neurons / Q000378:metabolism / Q000502:physiology; D020127:Recovery of Function / Q000235:genetics / Q000502:physiology*; D013117:Spinal Cord Compression / Q000150:complications*; D013119:Spinal Cord Injuries / Q000209:etiology / Q000235:genetics / Q000473:pathology / Q000503:physiopathology*; D019063:Tenascin / Q000172:deficiency; D013904:Thoracic Vertebrae; D013997:Time Factors; D050598:Vesicular Glutamate Transport Protein 1 / Q000378:metabolism; D050495:Vesicular Inhibitory Amino Acid Transport Proteins / Q000378:metabolism
chemical_list: D015815:Cell Adhesion Molecules; C490649:Chl1 protein, mouse; C493465:Slc17a7 protein, mouse; D019063:Tenascin; D050598:Vesicular Glutamate Transport Protein 1; D050495:Vesicular Inhibitory Amino Acid Transport Proteins; C492244:Viaat protein, mouse; C074638:tenascin R; D002795:Choline O-Acetyltransferase; D005998:Glycine