作者: Valerie M. K. Verge , Tracy D. Wilson-Gerwing , Laurie A. Karchewski , Kelly A. Gratto
DOI: 10.1007/978-3-0348-8129-6_3
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摘要: Peripheral nerve injury evokes a series of molecular, biochemical, and cyto-architectural changes in primary sensory neurons. These events, together with the injured corresponding regions spinal cord, contribute to repair processes neuropathic pain states that develop. Neuropathic is tremendous clinical problem, whereby normally innocuous or low-intensity stimuli acquire ability activate pathways. The goal basic research this area elucidate diverse events mechanisms responsible for state so more effective therapeutic interventions treatments may be developed. purpose chapter highlight aspects neuron response believed involved transition from normal nociception state. findings discussed stem largely two models peripheral — either complete sciatic transection most commonly used model pain, chronic constriction (CCI), which involves partial lesion induced by loosely tying chromic gut sutures [1]. latter results slow, edematous axotomy predominantly large diameter myelinated axons (90% As AS fibers 30% C three days post-ligation [2]), reproducible thermal mechanical allodynia, exposure uninjured Wallerian degenerating many proinflammatory molecules are produced.