Expression of fibroblast growth factor-2 in the nucleus ambiguus followingrecurrent laryngeal nerve injury in the rat

Citation
T. Sanuki et al., Expression of fibroblast growth factor-2 in the nucleus ambiguus followingrecurrent laryngeal nerve injury in the rat, LARYNGOSCOP, 110(12), 2000, pp. 2128-2134
Citations number
31
Categorie Soggetti
Otolaryngology
Journal title
LARYNGOSCOPE
ISSN journal
0023852X → ACNP
Volume
110
Issue
12
Year of publication
2000
Pages
2128 - 2134
Database
ISI
SICI code
0023-852X(200012)110:12<2128:EOFGFI>2.0.ZU;2-4
Abstract
Objectives: To examine fibroblast growth factor-a (FGF-2) immunoreactivity in the nucleus ambiguus (NA) after three different recurrent laryngeal nerv e (RLN) injuries. Study Design: Immunohistochemical analysis of FGF-2, Meth ods: Thirty adult rats underwent left-sided RLN crush (group A), The left R LN was transected in groups B (n = 30) and C (n = 30); in group C, both ner ve stumps mere covered with silicone caps. FGF-2 in the NA was assessed as the ratio of the positive areas on the Left (operated [O]) and right (unope rated [U]) sides. The ratio (O/U) was measured 1, 3, 7, 14, and 28 days aft er the procedure. Three rats underwent left-sided RLN exposure and mere kil led 7 days later (control). Results: Left-sided RLN paralysis occurred unti l day 28 in group k In the control group, O/U was approximately 1, In group A, O/Umas significantly elevated on day 7; in group B, on days 3, 7, and 1 4; and in group C, on day 3, O/U in group B was significantly greater than that in group A on days 14 and 28, Maximal FGF-2 immunoreactivity was signi ficantly lower in group C than in groups A and B, Conclusions: We demonstra ted elevated production of FGF-2 in the NA after RLN injury. This endogenou s FGF-2 might contribute to preventing lesion-induced neuronal death, Block age of axonal regeneration might suppress FGF-2 production in the Nk Furthe r understanding of the roles of FGF-2 after RLN injury may contribute to th e prevention of neuronal death and facilitation of axonal regeneration.