OBJECTIVE: To date, muscular and bone pain have been studied in domestic swine models, but the only neuropathic pain model described in swine is a mixed neuritis model. Common peroneal nerve injury (CPNI) neuropathic pain models have been utilized in both mice and rats. METHODS: The authors developed a swine surgical CPNI model of neuropathic pain. Behavioral outcomes were validated with von Frey filament testing, thermal sensitivity assessments, and social and motor scoring. Demyelination of the nerve was confirmed through standard histological assessment. The contralateral nerve served as the control. RESULTS: CPNI induced mechanical and thermal allodynia (p < 0.001 [n = 10] and p < 0.05 [n = 4], respectively) and increased pain behavior, i.e., guarding of the painful leg (n = 12). Myelin protein zero (P0) staining revealed demyelination of the ligated nerve upstream of the ligation site. CONCLUSIONS: In a neuropathic pain model in domestic swine, the authors demonstrated that CPNI induces demyelination of the common peroneal nerve, which the authors hypothesize is responsible for the resulting allodynic pain behavior. As the anatomical features of domestic swine resemble those of humans more closely than previously used rat and mouse models, utilizing this swine model, which is to the authors' knowledge the first of its kind, will aid in the translation of experimental treatments to clinical trials.
OBJECTIVE: To date, muscular and bone pain have been studied in domestic swine models, but the only neuropathic pain model described in swine is a mixed neuritis model. Common peroneal nerve injury (CPNI) neuropathic pain models have been utilized in both mice and rats. METHODS: The authors developed a swine surgical CPNI model of neuropathic pain. Behavioral outcomes were validated with von Frey filament testing, thermal sensitivity assessments, and social and motor scoring. Demyelination of the nerve was confirmed through standard histological assessment. The contralateral nerve served as the control. RESULTS: CPNI induced mechanical and thermal allodynia (p < 0.001 [n = 10] and p < 0.05 [n = 4], respectively) and increased pain behavior, i.e., guarding of the painful leg (n = 12). Myelin protein zero (P0) staining revealed demyelination of the ligated nerve upstream of the ligation site. CONCLUSIONS: In a neuropathic pain model in domestic swine, the authors demonstrated that CPNI induces demyelination of the common peroneal nerve, which the authors hypothesize is responsible for the resulting allodynic pain behavior. As the anatomical features of domestic swine resemble those of humans more closely than previously used rat and mouse models, utilizing this swine model, which is to the authors' knowledge the first of its kind, will aid in the translation of experimental treatments to clinical trials.
Authors: Ana-Maria Gaboreanu; Ronald Hrstka; Wenbo Xu; Michael Shy; John Kamholz; Jack Lilien; Janne Balsamo Journal: J Cell Biol Date: 2007-05-14 Impact factor: 10.539
Authors: Timothy R Deer; Robert M Levy; Jeffery Kramer; Lawrence Poree; Kasra Amirdelfan; Eric Grigsby; Peter Staats; Allen W Burton; Abram H Burgher; Jon Obray; James Scowcroft; Stan Golovac; Leonardo Kapural; Richard Paicius; Christopher Kim; Jason Pope; Thomas Yearwood; Sam Samuel; W Porter McRoberts; Hazmer Cassim; Mark Netherton; Nathan Miller; Michael Schaufele; Edward Tavel; Timothy Davis; Kristina Davis; Linda Johnson; Nagy Mekhail Journal: Pain Date: 2017-04 Impact factor: 7.926