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Ishihara, A., Ohira, Y., Tanaka, M., Nishikawa, W., Ishioka, N., Higashibata, A., Izumi, R., Shimazu, T. and Ibata, Y. (2001) Cell Body Size and Succinate Dehydrogenase Activity of Spinal Motoneurons Innervating the Soleus Muscle in Mice, Rats, and Cats. Neurochemical Research, 26, 1301-1304.
http://dx.doi.org/10.1023/A:1014245417017

has been cited by the following article:

• TITLE: Depletion of Glial Cell Line-Derived Neurotrophic Factor by Disuse Muscle Atrophy Exacerbates the Degeneration of Alpha Motor Neurons in Caudal Regions Remote from the Spinal Cord Injury

  AUTHORS: Yu-Ichiro Ohnishi, Koichi Iwatsuki, Toshiki Yoshimine

  KEYWORDS: Disuse Muscle Atrophy, Motor Neuron, Degeneration, Glial Cell Line-Derived Neurotrophic Factor

  JOURNAL NAME: Neuroscience and Medicine, Vol.5 No.5, November 24, 2014

  ABSTRACT: We have been previously reported that disuse muscle atrophy exacerbates both motor neuron (MN) degeneration in caudal regions remote from a spinal cord injury, and decrease in glial cell line-derived neurotrophic factor (GDNF) protein level in paralyzed muscle. In this study we found that disuse muscle atrophy exacerbated the decrease in GDNF protein level in the L4/5 spinal cord, which was not immunopositive for GDNF. Our results were consistent with the fact that in the lumbar spinal cord of rats with mid-thoracic contusion, GDNF expression was not detected, while expression of GDNF receptors (GFRα1 and RET) was. Our study showed that administration of exogenous recombinant GDNF into the atrophic muscle partially rescued α-MN degeneration in the L4/5 spinal cord. These results suggest that the depletion of GDNF protein by muscle atrophy exacerbates α-MN degeneration in caudal regions remote from the injury.