INCREASED CU/ZN SUPEROXIDE DISMUTASE-LIKE IMMUNOREACTIVITY IN THE SWOLLEN AXONS OF RATS INTOXICATED CHRONICALLY WITH BETA,BETA'-IMINODIPROPIONITRILE

被引：12

作者：

NISHIYAMA, K ^{[1
]}

KWAK, S ^{[1
]}

MURAYAMA, S ^{[1
]}

WATANABE, M ^{[1
]}

GOTO, J ^{[1
]}

ASAYAMA, K ^{[1
]}

KANAZAWA, I ^{[1
]}

机构：

[1] YAMANASHI MED COLL, DEPT PEDIAT, YAMANASHI, JAPAN

来源：

NEUROSCIENCE LETTERS | 1995年 / 194卷 / 03期

关键词：

BETA; BETA'-IMINODIPROPIONITRILE; CU/ZN SUPEROXIDE DISMUTASE; RAT; SWOLLEN AXON; IMMUNOCYTOCHEMISTRY; IN SITU HYBRIDIZATION;

D O I：

10.1016/0304-3940(95)11762-L

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Demonstration of a genetic linkage between the Cu/Zn superoxide dismutase (SOD1) gene and familial amyotrophic lateral sclerosis (ALS) has aroused interest in the role of SOD1 in spinal motoneuronal death. We used chronically beta,beta'-iminodipropionitrile (IDPN)intoxicated rats as a model of ALS and investigated SOD1 changes in the spinal cord by immunocytochemical and in situ hybridization techniques. Compared with control rats, SOD1-Like immunoreactivity (SOD1-IR) increased in swollen axons of the proximal spinal roots, but not in motoneuronal and dorsal root ganglion neuronal cell bodies where SOD1 gene transcription did not increase, The present data indicate that treatment with IDPN induces accumulation of SOD1 in the swollen axons by blocking slow axonal flow, suggesting the possibility that increased SOD1-IR in ALS is induced by axonal flow blockade.

引用

页码：205 / 208

页数：4

共 17 条

[1] THE IMINODIPROPIONITRILE (IDPN)-INDUCED DYSKINETIC SYNDROME - BEHAVIORAL AND BIOCHEMICAL PHARMACOLOGY [J].