Changes in gene expression in facial nerve nuclei in the rat model of ischemic Bell's palsy

1997 Fiscal Year Final Research Report Summary

• Project/Area Number: 08671997
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Otorhinolaryngology
• Research Institution: Hyogo College of Medicine
• Principal Investigator: SEO Toru Hyogo College of Medicine, Instructor, 医学部, 助手 (30258149)
• Co-Investigator(Kenkyū-buntansha): NOGUCHI Koichi Hyogo College of Medicine, Professor, 医学部, 教授 (10212127) ; SATOMI Fumio Hyogo College of Medicine, Assistant Professor, 医学部, 講師 (20248149)
• Project Period (FY): 1996 – 1997
• Keywords: peripheral facial nerve paralysis / in situ hybridization / CGRP / c-jun / GAP-43 / SOD

Research Abstract

It is well known that expression of CGRP (calcitonin gene-related peptide) , c-jun (immediate early gene) and GAP-43 (growth-associated protein, B-50) mRNAs increase in the rat facial nerve nuclei after peripheral nerve injury. Direct damage to the nerve is supposed to induce changes in gene expression of these neuroactive substances, which may have roles in adaptive response to the injury, neuronal survival, growth and regeneration. This study was designed to establish ischemic animal model of peripheral facial nerve paralysis with a selective embolization technique. In this model, the paralysis of facial continued for about 3 days and recovered without any neuronal deficit. We observed the levels in CGRP,c-jun and GAP-43 mRNAs in facial nerve nuclei using in situ hybridization. The increase of these mRNA appeared one day after embolization, lasted for 1 week and gradually decreased. The results suggest that the expression of CGRP,c-jun and GAP-43 in cell somata is induced by ischemic facial nerve paralysis, and the level and duration of increase in these mRNAs are different from those in direct nerve injury model.