Immunohistochemical Study on the Distribution of Glycogen Synthase Kinase (GSK) 3beta in the Central Nervous System of SOD1G93A Transgenic Mice.
10.11637/kjpa.2007.20.4.355
- Author:
Kyeung Min JOO
1
;
Yoon Hee CHUNG
;
Sung Su KIM
;
Kyung Yong KIM
;
Won Bok LEE
;
Choong Ik CHA
Author Information
1. Department of Anatomy, College of Medicine, Seoul National University, Korea. cicha@snu.ac.kr
- Publication Type:Original Article
- Keywords:
Glycogen synthase kinase (GSK) 3beta;
Amyotrophic lateral sclerosis (ALS);
SOD1G93A transgenic mice;
Spinal cord;
Brain stem;
Cerebellum
- MeSH:
Amyotrophic Lateral Sclerosis;
Animals;
Brain Stem;
Central Nervous System*;
Cerebellum;
Glycogen Synthase Kinases*;
Glycogen Synthase*;
Glycogen*;
Humans;
Mice;
Mice, Transgenic*;
Neurons;
Spinal Cord;
Superoxide Dismutase
- From:Korean Journal of Physical Anthropology
2007;20(4):355-362
- CountryRepublic of Korea
- Language:English
-
Abstract:
In the present study, we investigated influences of glycogen synthase kinase (GSK) 3beta on the development and/or progression of amyotrophic lateral sclerosis (ALS). We used transgenic mice expressing a human Cu/Zn superoxide dismutase mutant (SOD1G93A) as an in vivo model of ALS and examined expressional changes of GSK3beta immunohistochemically in the spinal cord, brain stem and cerebellum. With these experiments we demonstrate that the neurons in these regions of symptomatic SOD1G93A transgenic mice showed increased GSK3beta immunoreactivities compared with wild-type SOD1 transgenic mice. In contrast to symptomatic SOD1G93A transgenic mice, few GSK3beta immunoreactivity changes were detected in 8w- and 13w-old presymptomatic SOD1G93A transgenic mice. These data suggest the possibility that GSK3 functions as a modulating factor of apoptosis-related alterations in ALS and that GSK3beta exert differential functions in the development and/or progression of ALS. But the exact functional significances of these changes require further elucidation.
