Passive exercise of the hind limbs after complete thoracic transection of the spinal cord promotes cortical reorganization.
Physical exercise promotes neural plasticity in the brain of healthy subjects and modulates pathophysiological neural plasticity after sensorimotor loss, but the mechanisms of this action are not fully understood. After spinal cord injury, cortical reorganization can be maximized by exercising the non-affected body or the residual functions of the affected body. However, exercise per se also produces systemic changes - such as increased cardiovascular fitness, improved circulation and neuroendocrine changes - that have a great impact on brain function and plasticity. It is therefore possible that passive exercise therapies typically applied below the level of the lesion in patients with spinal cord injury could put the brain in a more plastic state and promote cortical reorganization. To directly test this hypothesis, we applied passive hindlimb bike exercise after complete thoracic transection of the spinal cord in adult rats. Using western blot analysis, we found that the level of proteins associated with plasticity - specifically ADCY1 and BDNF - increased in the somatosensory cortex of transected animals that received passive bike exercise compared to transected animals that received sham exercise. Using electrophysiological techniques, we then verified that neurons in the deafferented hindlimb cortex increased their responsiveness to tactile stimuli delivered to the forelimb in transected animals that received passive bike exercise compared to transected animals that received sham exercise. Passive exercise below the level of the lesion, therefore, promotes cortical reorganization after spinal cord injury, uncovering a brain-body interaction that does not rely on intact sensorimotor pathways connecting the exercised body parts and the brain.
Department of Physiology and Pharmacology, Drexel University College of Medicine, Philadelphia, Pennsylvania, USA. Alessandro.Graziano@DrexelMed.edu
Alessandro
A
Graziano
Guglielmo
G
Foffani
Eric B
EB
Knudsen
Jed
J
Shumsky
Karen A
KA
Moxon
D000262:Adenylyl Cyclases / Q000378:metabolism / Q000502:physiology; D000818:Animals; D000831:Animals, Newborn; D001931:Brain Mapping; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism / Q000502:physiology; D002540:Cerebral Cortex / Q000503:physiopathology*; D015444:Exercise; D006614:Hindlimb / Q000378:metabolism / Q000502:physiology; D006801:Humans; D009473:Neuronal Plasticity / Q000502:physiology; D009474:Neurons / Q000378:metabolism / Q000502:physiology; D010805:Physical Conditioning, Animal / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013003:Somatosensory Cortex / Q000503:physiopathology; D013116:Spinal Cord / Q000503:physiopathology; D013119:Spinal Cord Injuries / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy*
D019208:Brain-Derived Neurotrophic Factor; D000262:Adenylyl Cyclases; C106670:adenylyl cyclase 1