Brain-dependent movements and cerebral-spinal connections: Key targets of cellular and behavioral enrichment in CNS injury models
Journal of rehabilitation research and development
One of the most difficult problems in experimental and clinical neurology is how to facilitate recovery of the ability to walk voluntarily. Local spinal mechanisms, descending input from the brain, and ascending sensory feedback to the brain are required for non-treadmill, self-initiated stepping. In evaluating the integrity of axons connecting the brain and spinal cord in neural injury models, the selection of behavioral tests may be at least as important as the histological procedures, if not
... procedures, if not more so. A comprehensive and clinically meaningful test battery should include assessments of brain-dependent movement capacity. Behavioral enrichment procedures that prominently encourage self-initiation of stepping have been used to facilitate plasticity and motor function after brain or spinal cord injury. Progressive degeneration characteristic of parkinsonian models can be slowed or halted altogether by forced exercise and limb use. Behavioral interventions may work partly because the animal adopts alternative behavioral strategies to compensate for impaired performance. However, mounting evidence suggests that motor rehabilitation can also promote restoration of function or prevent slow degeneration of tissue by engaging constitutively available mechanisms that protect, repair, rewire, or reactivate cells. Abbreviations: BDNF = brain-derived neurotrophic factor, CNS = central nervous system, FGF-2 = fibroblast growth factor 2, GDNF = glial-derived neurotrophic factor, MPTP = 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, NMDA = N-methyl-Daspartate, 6-OHDA = 6-hydroxydopamine.