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Sprouting and reorganization in the spinal cord after nerve injury

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Mechanisms and Mediators of Neuropathic Pain

Part of the book series: Progress in Inflammation Research ((PIR))

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Abstract

Several different nerve injury models were introduced in the last decades of the 20th century. These include the chronic constriction injury (CCI) or “Bennett” model in which the entire sciatic nerve is loosely ligated with chromic gut suture [1], the partial nerve ligation (PNL) or “Seltzer” model in which 1/3-1/2 of the axons in the sciatic nerve are tightly ligated [2] and the spinal nerve ligation (SNL) or “Chung” model in which the L5 and L6 spinal nerves are tightly ligated [3]. The major advantage these models have over the more commonly used simple sciatic nerve transection is that, unlike sciatic transection, some fibers are still in contact with the periphery within the sciatic distribution. Thus, behavioral testing can be performed in this region of the nerve injured limb to allow assessments of changes in mechanical and thermal sensitivity. The ability to correlate changes in dorsal horn morphology and neurochemistry with behavioral status led to a multitude of studies attempting to obtain insights into changes in spinal cord neurocircuitry that underlie the observed nociceptive behaviors. Although other nerve-injury models exist, the central reorganization of primary afferent fibers [4] or the pain behaviors [5] have not yet been well characterized.

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Carlton, S.M., Coggeshall, R.E. (2002). Sprouting and reorganization in the spinal cord after nerve injury. In: Malmberg, A.B., Chaplan, S.R. (eds) Mechanisms and Mediators of Neuropathic Pain. Progress in Inflammation Research. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-8129-6_6

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