Exercise Modulates Chloride Homeostasis after Spinal Cord Injury

• DOI: 10.1523/jneurosci.0678-14.2014
• Publication Date: 2014-07-02T16:36:42Z
• Authors: M.-P. Cote; S. Gandhi; M. Zambrotta; J. D. Houle
• Keywords: Hyperreflexia; Homeostasis

Activity-based therapies are routinely integrated in spinal cord injury (SCI) rehabilitation programs because they result a reduction of hyperreflexia and spasticity. However, the mechanisms by which exercise regulates activity pathways to reduce spasticity improve functional recovery poorly understood. Persisting alterations action GABA on postsynaptic targets is signature CNS injuries, including SCI. The depends intracellular chloride concentration, determined largely expression two cation-chloride cotransporters (CCCs), KCC2 NKCC1, serve as exporters importers, respectively. We hypothesized that with after SCI relies return homeostasis. Sprague Dawley rats received transection at T12 were assigned SCI-7d, SCI-14d, SCI-14d+exercise, SCI-28d, SCI-28d+exercise, or SCI-56d groups. During terminal experiment, H-reflexes recorded from interosseus muscles stimulation tibial nerve low-frequency-dependent depression (FDD) was assessed. provide evidence returns excitability levels NKCC1 toward normal lumbar cord. Acutely altering extrusion using blocker DIOA masked effect FDD, whereas blocking bumetanide returned FDD intact Our results indicate contributes reflex restoration endogenous inhibition through homeostasis This lends support for CCCs part pathway could be manipulated when combined programs.