Effect Of Long-Term Exercise On GDNF Expression And Innervation In Rat Skeletal Muscle
Exercise provides neuroprotection by promoting neurogenesis, decreasing apoptosis, and modulating inflammation; however, the mechanism is not well understood. GDNF is a neurotrophic factor that has been shown to be a potent survival factor for somatic motor neurons that innervate skeletal muscle, but GDNF levels in muscle decrease with aging. Our hypothesis is that long-term exercise will increase GDNF expression, and support NMJ structures. Adult Sprague-Dawley rats were exercised by voluntary running for 6 months. Age-matched sedentary group maintained in cages without access to running wheels served as controls. After 6 months, hind-limb muscles were collected and processed for GDNF protein content via ELISA. Motor end plates were stained with a-bungarotoxin, and anti-GDNF was used to detect GDNF. There was a significant increase in length of end plates in muscles from exercised rats (36.6 ± 3.5um), and a significant increase in area (616.3 ± 84.9um^2) of stained end plates in muscles from exercised rats compared to length (27.6 ± 1.15um) and area (430.3 ± 30.8um^2) of the control group. There was a trend towards an increase in GDNF protein content in muscle from exercised rats; however, the effect was not significant. Findings suggest that increased physical activity enhances structural neuroplasticity in NMJ elements and may possibly lead to enhanced neuromuscular function. Understanding the activity dependent regulation of neurotrophic factor expression and neural plasticity in the neuromuscular system may help in identifying novel targets for pharmacological development.