Fernandez H L, Hodges-Savola C A
Neuroscience Research Laboratory, U.S. Department of Veterans Affairs Medical Center, Kansas City, Missouri 64128.
Neurochem Res. 1992 Jan;17(1):115-24. doi: 10.1007/BF00966872.
This work addresses the physiological regulation of skeletal muscle acetylcholinesterase (AChE) isoforms by examining endplate-enriched samples from adult rat gracilis muscles 48 h after: low-intensity treadmill exercise; obturator nerve transection; nerve impulse conduction blockade by tetrodotoxin; acetylcholine (ACh) receptor (AChR) inactivation by alpha-bungarotoxin; and, addition of obturator nerve extracts to muscles in organ culture. Results document the important role(s) of functional AChRs and ACh-AChR interactions in the differential control of individual AChE isoenzymes. A theoretical model based on these and other findings considers that: AChR activation by spontaneously released ACh is the only neural factor required for the maintenance of G1 + G2 AChE; the amount of A12 AChE is determined by the combined effects of ACh and another neurogenic substance; although mechanisms intrinsic to myofibers control normal levels of G4 AChE, enhanced production of this isoform is initiated through increasing the frequency of ACh-AChR interactions.
本研究通过检测成年大鼠股薄肌终板富集样本，探讨了骨骼肌乙酰胆碱酯酶（AChE）同工型的生理调节机制，样本取自以下处理48小时后的肌肉：低强度跑步机运动；闭孔神经横断；河豚毒素阻断神经冲动传导；α-银环蛇毒素使乙酰胆碱（ACh）受体（AChR）失活；以及在器官培养中将闭孔神经提取物添加到肌肉中。结果证明了功能性AChR和ACh-AChR相互作用在个体AChE同工酶差异调控中的重要作用。基于这些及其他发现的理论模型认为：自发释放的ACh激活AChR是维持G1 + G2 AChE所需的唯一神经因素；A12 AChE的量由ACh和另一种神经源性物质的联合作用决定；虽然肌纤维内在机制控制着G4 AChE的正常水平，但该同工型产量的增加是通过增加ACh-AChR相互作用的频率启动的。
