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The effects of exercise on skeletal muscle GSK3β in a spinal cord injury pain model
Author(s) -
Jones Terry E.,
Wood Melissa K.,
Brewer Kori L.,
Bareiss Sonja K.
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1086.5
Subject(s) - spinal cord injury , medicine , spinal cord , glycogen , skeletal muscle , endocrinology , citrate synthase , central nervous system , soleus muscle , chemistry , biochemistry , enzyme , psychiatry
Spinal cord injury (SCI) causes central and peripheral nervous system changes in glycogen synthase kinase 3β (GSK3β) activity. This protein is expressed in skeletal muscle and is reported to decrease in activity with aerobic training. The objective was to determine the content of total and phosphorylated GSK3β (pGSK3β) in muscle from spinal cord injured (SCI) rats and if exercise altered their content. Rats were randomly assigned to control (CON), sedentary (SCI), or exercise groups (SCI/Ex). The SCI and SCI/Ex group underwent excitotoxic SCI injury (a chronic pain model) while CON underwent a saline injection. Animals were treadmill exercised for 12 days. Soleus muscles were excised. Muscle homogenates were used for Western blot analysis probing for total GSK3β and pGSK3β. The protein content of total GSK3β was significantly decreased 30% in SCI/Ex compared to control and SCI. pGSK3β was not significantly different between groups but was reduced 13% and 29% between control and SCI or SCI/Ex, respectively, suggesting a potential increase in activity. These results suggest that GSK3β may be regulated in an alternative fashion in a chronic pain model. The Wooten Laboratory for Neurodegenerative Disease Research supports this work.