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Motoneuron degeneration after facial nerve avulsion is exacerbated in presymptomatic transgenic rats expressing human mutant Cu/Zn superoxide dismutase
Author(s) -
Ikeda Ken,
Aoki Masashi,
Kawazoe Yoko,
Sakamoto Tsuyoshi,
Hayashi Yuichi,
Ishigaki Aya,
Nagai Makiko,
Kamii Rieko,
Kato Shinsuke,
Itoyama Yasuto,
Watabe Kazuhiko
Publication year - 2005
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.20621
Subject(s) - axotomy , immunolabeling , endocrinology , medicine , superoxide dismutase , avulsion , sod1 , pathology , anatomy , oxidative stress , immunohistochemistry , central nervous system
We investigated motoneuron degeneration after proximal nerve injury in presymptomatic transgenic (tg) rats expressing human mutant Cu/Zn superoxide dismutase (SOD1). The right facial nerves of presymptomatic tg rats expressing human H46R or G93A SOD1 and their non‐tg littermates were avulsed, and facial nuclei were examined at 2 weeks postoperation. Nissl‐stained cell counts revealed that facial motoneuron loss after avulsion was exacerbated in H46R‐ and G93A‐tg rats compared with their non‐tg littermates. The loss of motoneurons in G93A‐tg rats after avulsion was significantly greater than that in H46R‐tg rats. Intense cytoplasmic immunolabeling for SOD1 in injured motoneurons after avulsion was demonstrated in H46R‐ and G93A‐tg rats but not in their littermates. Facial axotomy did not induce significant motoneuron loss nor enhance SOD1 immunoreactivity in these tg rats and non‐tg littermates at 2 weeks postoperation, although both axotomy and avulsion elicited intense immunolabeling for activating transcription factor‐3, phosphorylated c‐Jun, and phosphorylated heat shock protein 27 in injured motoneurons of all these animals. The present data indicate the increased vulnerability of injured motoneurons after avulsion in the presymptomatic mutant SOD1‐tg rats. © 2005 Wiley‐Liss, Inc.