• Shannon D Shields, William A Eckert, and Allan I Basbaum.
• Department of Anatomy, University of California-San Francisco, San Francisco, California, USA.
• J Pain. 2003 Oct 1; 4 (8): 465-70.

AbstractMouse genetics has contributed significantly to our understanding of molecular mechanisms underlying tissue and nerve injury-induced persistent pain. To create a highly reproducible, relatively noninvasive model of neuropathic pain in the mouse, we examined the behavioral consequences of sparing each of the 3 distal branches of the sciatic nerve in wild-type mice after a model originally described in the rat. Sparing the tibial branch but sparing neither of the other branches produced robust mechanical allodynia while leaving heat sensibility intact. To assess the topographic organization of the IB4 population of afferents from each branch and to compare anatomic consistency across injury models, we examined loss of thiamine monophosphatase staining in the superficial dorsal horn after peripheral nerve injury. We found that each of the sciatic branches targets a distinct mediolateral location in inner lamina II and that each of the spared nerve injury models produced a more reproducible pattern of thiamine monophosphatase staining loss than did partial tight ligation. These results improve on previous nerve injury models in mouse, demonstrate similar behavioral changes as in rat, and provide novel information on the topographic organization of small diameter peripheral afferents in the mouse spinal cord.

32 keywords...

hide…