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Beneficial effect of melatonin and forced exercise on degeneration of lower motor neuron after focal cerebral ischemia in rats
Author(s) -
Lee Seunghoon,
Hong Yunkyung,
Hong Yonggeun
Publication year - 2013
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.27.1_supplement.940.15
Subject(s) - motor neuron , medicine , neuron , melatonin , ischemia , spinal cord , lesion , endocrinology , atrophy , anesthesia , pathology , psychiatry
The stroke lesion primarily affects the territory of the upper motor neuron, but these clinical signs take shape by means of the skeletal muscle controlled by the lower motor neuron. Therefore, we elucidated that melatonin and exercise is a possible intervention on the rescue of lower motor neuron degeneration after focal cerebral ischemia. Following the MCAo, the 8‐week‐old Sprague‐Dawley (SD) rats were treated twice daily with MT (10 mg/kg) at 7:00 and 19:00 hr and control group were treated with physiological saline (vehicle) instead of MT. Also, the rats were trained twice daily with Ex (20 m/min) at 17:00 and 22:00 hr. MT+Ex is significantly inhibited the attenuation of lower motor neuron during 7 days in both cervical and lumbar spinal cord (p<0.01). Analysis of gene expression in gastroncnemius, MT+Ex is not only downregulated the atrophy‐related genes, including MuRF1 and MAFbx but also upregulated the hypertrophic signal upstream molecule, such as IGF‐1 via overexpression of IGF‐1R (p<0.05, p<0.01, respectively). Moreover, there is significantly inhibited the reduction of muscle fiber diameter following MT and MT+Ex (p<0.01). In here, we found that melatonin and forced exercise could be suppressed the lower motor neuron degeneration as well as stroke‐induced muscle atrophy on early stage after MCAo. Accordingly, we suggest that melatonin has a possible rehabilitative agent as well as the synergistic effect with therapeutic exercise.