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Involuntary exercise is a better stimulus than voluntary exercise to increase GDNF protein content in adult rat spinal cord
Author(s) -
McCullough Monica Janine,
Gyorkos Amy M,
Spitsbergen John M
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.1142.33
Subject(s) - glial cell line derived neurotrophic factor , neurotrophic factors , spinal cord , medicine , endocrinology , central nervous system , neuroscience , spinal cord injury , turnover , motor neuron , physical medicine and rehabilitation , psychology , receptor , management , economics
Glial cell line‐derived neurotrophic factor (GDNF) is the most potent neurotrophic factors for motor neurons. We have previously shown that short term involuntary exercise alters GDNF protein content in rat skeletal muscle, yet, little is known about how exercise regulates GDNF in the spinal cord of healthy individuals. The aim of the current study was to examine changes in GDNF protein content in the spinal cord from adult rats following involuntary and voluntary exercise of different durations. Male Sprague Dawley rats aged 6 to 24 months were examined. Exercised animals were placed into groups of either voluntary running wheels, involuntary running wheels, or forced swimming. Age‐matched control animals had no exposure to exercise. GDNF protein content of the spinal cord was measured using an ELISA and western blot. Immunohistochemistry localized GDNF and examined motor neuron morphology. Two weeks of involuntary running resulted in the greatest change in GDNF protein content (6.5‐fold increase) whereas 6 months of voluntary running decreased GDNF protein content (0.8‐fold decrease). Short‐term involuntary exercise may be better than long‐term voluntary exercise to increase GDNF in the spinal cord of aging individuals and provide neuroprotection of the motor nervous system with aging. This work was supported by NIH grant 1 R15 AG022908‐ 01A2, NSF grant DBI 0552517, Western Michigan University, and MSU‐KCMS.