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