Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0599766 (functional recovery)
 13,441 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Better functional outcome of compression spinal cord injury in mice is associated with enhanced H-reflex responses. 1915 Jun 14

Mice deficient in the recognition molecules, close homolog of L1 (CHL1) and tenascin-C, show improved and reduced functional recovery, respectively, after spinal cord injury compared with wild-type littermates. In this study, we addressed the question whether the differential functional outcome was paralleled by differences in blood-spinal cord barrier (BSCB) repair in the two mouse strains. We conducted spinal cord compression injuries in knock-out and wild-type mice. BSCB permeability was assessed by measuring the Evans blue spread within the spinal cord tissue at 14-21 days after injury. Results show that CHL1 reduces and tenascin-C enhances BSCB permeability, suggesting a correlation between functional outcome and BSCB repair.
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PMID:Adhesion molecules close homolog of L1 and tenascin-C affect blood-spinal cord barrier repair. 2247 92