Abstract
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.
Highlights
Limb amputation, damage to peripheral nerves and spinal cord injury can alter the somatotopic organization of the primary somatosensory cortex [1,2,3,4,5,6]
We performed western blot analysis to assess the levels of plasticity-related proteins in the somatosensory cortex of 32 rats, divided in 5 groups (Fig. 1A): one group of normal animals (n = 6); two groups of ‘bike-exercise’ transected animals, which received either 1 week (n = 8) or 8 weeks (n = 5) of hindlimb bike exercise after complete thoracic (T9/T10) transection of the spinal cord; two groups of ‘sham-exercise’ transected animals, which received either 1 week (n = 7) or 8 weeks (n = 6) of sham bike exercise after the spinal cord transection
Passive hindlimb bike exercise or sham bike exercise started the week after the spinal transection and animals were sacrificed within one hour after the last session
Summary
Damage to peripheral nerves and spinal cord injury can alter the somatotopic organization of the primary somatosensory cortex [1,2,3,4,5,6]. Cortical reorganization after somatosensory deafferentation can lead to the enlargement of cortical representations of intact body areas into cortical representations of deafferented body areas. A natural strategy to maximize cortical reorganization after somatosensory deafferentation is to increase the activity of the intact cortex by exercising the non-affected body or the residual functions of the affected body, as investigated in previous works in rat models [9,21,22] and in patients with spinal cord injury [23,24,25,26]. An alternative strategy would be to put the overall cortex in a more plastic state, e.g. using systemic drugs or other manipulations that generically promote cortical plasticity [27,28,29]
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