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Expression of Fibroblast Growth Factor‐2 in the Nucleus Ambiguus Following Recurrent Laryngeal Nerve Injury in the Rat
Author(s) -
Sanuki Tetsuji,
Yumoto Eiji,
Komori Masahiro,
Hyodo Masamitsu
Publication year - 2000
Publication title -
the laryngoscope
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.181
H-Index - 148
eISSN - 1531-4995
pISSN - 0023-852X
DOI - 10.1097/00005537-200012000-00030
Subject(s) - nucleus ambiguus , recurrent laryngeal nerve , medicine , lesion , fibroblast growth factor , immunohistochemistry , anesthesia , endocrinology , surgery , anatomy , central nervous system , medulla oblongata , thyroid , receptor
Objectives To examine fibroblast growth factor‐2 (FGF‐2) immunoreactivity in the nucleus ambiguus (NA) after three different recurrent laryngeal nerve (RLN) injuries. Study Design Immunohistochemical analysis of FGF‐2. Methods Thirty adult rats underwent left‐sided RLN crush (group A). The left RLN was transected in groups B (n = 30) and C (n = 30); in group C, both nerve stumps were 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 (unoperated [ U ]) sides. The ratio ( O/U ) was measured 1, 3, 7, 14, and 28 days after the procedure. Three rats underwent left‐sided RLN exposure and were killed 7 days later (control). Results Left‐sided RLN paralysis occurred until day 28 in group A. In the control group, O/U was approximately 1. In group A, O/U was significantly elevated on day 7; in group B, on days 3, 7, and 14; 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 significantly lower in group C than in groups A and B. Conclusions We demonstrated elevated production of FGF‐2 in the NA after RLN injury. This endogenous FGF‐2 might contribute to preventing lesion‐induced neuronal death. Blockage of axonal regeneration might suppress FGF‐2 production in the NA. Further understanding of the roles of FGF‐2 after RLN in‐jury may contribute to the prevention of neuronal death and facilitation of axonal regeneration.