• Elena Redondo-Castro, Guillermo García-Alías, and Xavier Navarro.
• Group of Neuroplasticity and Regeneration, Institute of Neurosciences and Department of Cell Biology, Physiology and Immunology, Universitat Autònoma de Barcelona, Spain.
• Restor. Neurol. Neurosci. 2013 Jan 1;31(4):411-30.

PurposeSpinal cord injuries (SCI) cause motor, sensory and autonomic dysfunctions as well as neuropathic pain. We investigated plastic changes occurring in cord segments caudal to the lesion to assess their potential contribution to pain states after SCI.MethodsDifferent thoracic SCIs were performed in adult rats. Functional and algesimetry tests were performed along 3 months. Several elements of the spinal nociceptive circuitry were assessed by immunohistochemical analyses of lumbar segments.ResultsInjured animals manifested mechanical and thermal hyperalgesia. Wind-up responses and spinal reflexes were enhanced, indicating spinal hyperexcitability. We found an increase in density of nociceptive sensory afferences and in GABA inhibitory activity in dorsal horns, and increased glial reactivity. Serotoninergic descending fibers and contacts on ventral horn motoneurons were reduced. Motoneurons presented more abundant inhibitory inputs, identified by gephyrin. Not all the changes kept direct relationship to the severity of the injury.ConclusionThe existence of hyperalgesia despite the boost of inhibitory elements in the spinal cord confirms the dysbalance between excitatory and inhibitory mechanisms, leading to a general disinhibition. Widespread dysfunctions in remote segments after central injuries contribute to the appearance of pain, and they may be new targets for therapies aimed to modulate spinal dysfunctions after injury.

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