Role of chloride cotransporters in the development of spasticity and neuropathic pain after spinal cord injury

Abstract Chloride homeostasis is critically involved in motor and sensory processing in the spinal cord. After spinal cord injury, spinal networks are hyperexcitable leading to increased transmission in both nociceptive and proprioceptive pathways. It was recently shown that the emergence of chronic pain and spasticity after SCI is not only due to increased excitation resulting from impaired or lost supraspinal inhibitory drive, but also to a lack of endogenous GABAergic inhibition triggered by a shift in chloride homeostasis. This chapter will cover the development of chloride homeostasis in the spinal cord, the effect of spinal cord injury on chloride cotransporters, the functional consequences and, the promising therapeutic strategies.