Western Michigan University, Department of Biological Sciences, 1903 W. Michigan Avenue, Kalamazoo, MI 49008-5410, USA.
Neuroscience. 2011 Feb 3;174:234-44. doi: 10.1016/j.neuroscience.2010.11.016. Epub 2010 Nov 23.
Current evidence suggests that exercise and glial cell line-derived neurotrophic factor (GDNF) independently cause significant morphological changes in the neuromuscular system. The aim of the current study was to determine if increased physical activity regulates GDNF protein content in rat skeletal muscle. Extensor Digitorum Longus (EDL) and Soleus (SOL) hind limb skeletal muscles were analyzed following 2 weeks of involuntary exercise and 4 h of field stimulation or stretch in muscle bath preparations. GDNF protein content was measured via enzyme-linked immunosorbent assay (ELISA). Two weeks of exercise increased GDNF protein content in SOL as compared to sedentary controls (4.4±0.3 pg GDNF/mg tissue and 3.1±0.6 pg GDNF/mg tissue, respectively) and decreased GDNF protein content in EDL as compared to controls (1.0±0.1 pg GDNF/mg tissue and 2.3±0.7 pg GDNF/mg tissue, respectively). GDNF protein content in the EDL decreased following both field stimulation (56%±18% decrease from controls) and stretch (66%±10% decrease from controls). SOL responded to field stimulation with a 38%±7% increase from controls in GDNF protein content, but showed no change following stretch. Pre-treatment with α-bungarotoxin abolished the effects of field stimulation in both muscles and blocked the effect of stretch in EDL. α-bungarotoxin pre-treatment and stretch increased GDNF protein content to 240%±10% of controls in the SOL. Exposure to carbamylcholine decreased GDNF protein content to 51%±28% of controls in the EDL but not SOL. These results suggest that GDNF protein content in skeletal muscle may be controlled by stretch, where it may increase GDNF protein content, and membrane depolarization/acetylcholine (ACh) which acts to decrease GDNF protein content.
目前的证据表明,运动和胶质细胞源性神经营养因子(GDNF)独立地引起神经肌肉系统的显著形态变化。本研究的目的是确定增加身体活动是否调节大鼠骨骼肌中的 GDNF 蛋白含量。在肌肉浴制剂中进行 2 周的非自愿运动和 4 小时的场刺激或拉伸后,分析伸趾长肌(EDL)和比目鱼肌(SOL)后肢骨骼肌。通过酶联免疫吸附测定(ELISA)测量 GDNF 蛋白含量。与久坐对照组相比,2 周的运动增加了 SOL 中的 GDNF 蛋白含量(分别为 4.4±0.3 pg GDNF/mg 组织和 3.1±0.6 pg GDNF/mg 组织),并降低了 EDL 中的 GDNF 蛋白含量(分别为 1.0±0.1 pg GDNF/mg 组织和 2.3±0.7 pg GDNF/mg 组织)。EDL 中的 GDNF 蛋白含量在场刺激(对照减少 56%±18%)和拉伸(对照减少 66%±10%)后均下降。SOL 对场刺激的反应是 GDNF 蛋白含量增加 38%±7%,而拉伸后没有变化。α-银环蛇毒素预处理消除了两种肌肉中的场刺激作用,并阻断了 EDL 中的拉伸作用。α-银环蛇毒素预处理和拉伸使 SOL 中的 GDNF 蛋白含量增加到对照的 240%±10%。暴露于氨甲酰胆碱使 EDL 中的 GDNF 蛋白含量降低至对照的 51%±28%,但 SOL 中没有。这些结果表明,骨骼肌中的 GDNF 蛋白含量可能受到拉伸的控制,拉伸可能增加 GDNF 蛋白含量,以及膜去极化/乙酰胆碱(ACh),其作用是降低 GDNF 蛋白含量。