• Safa Aldeen S Shehab.
• Department of Anatomy, Faculty of Medicine and Health Sciences, United Arab Emirates University, Al-Ain, United Arab Emirates. s.shehab@uaeu.ac.ae
• J. Comp. Neurol. 2009 Dec 1; 517 (4): 481-92.

AbstractThe mechanism of neuropathic pain may be associated with sprouting of uninjured primary afferents of peripheral nerves into regions of the spinal cord denervated through peripheral injury. However, this remains controversial. Therefore, the purpose of the present investigation was, first, to determine in detail the central distributions of the unmyelinated primary afferents of each of the L4, L5, and L6 components of sciatic nerve, then to assess the distribution of afferent sciatic terminals following acute and chronic injury to (L5) nerve. First, we injected isolectin B4 (IB4), into the sciatic nerves in three groups of rats, each of which had two of the three L4, L5, or L6 components ligated and cut, and the one remaining, uninjured. Although the terminal labelling found in the L5 segment of the spinal cord originated from the L5 component, some terminal labelling remained in cases when either the L4 or L6 component was intact. Second, tracers transported in predominantly unmyelinated (IB4 and WGA-HRP) or myelinated (cholera toxin subunit B) nerves were injected into the sciatic nerve following acute or chronic (21-day) injury restricted to the L5 component. In each case, the central distribution of nerve terminals in the spinal dorsal horn was equivalent following either acute or chronic injury to the L5 component. Consequently, these data provide no support for the suggestion that neuropathic pain in spinal ligation model results from uninjured L4 and L6 components sprouting to occupy sites vacated by the injured L5 component of the sciatic nerve.

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