Howlett S E, Hoekman T B
Exp Neurol. 1986 Nov;94(2):416-25. doi: 10.1016/0014-4886(86)90114-7.
In the avian model of muscular dystrophy, electrophysiologic studies have shown alterations in the action potential characteristics of dystrophic muscle in vitro, supporting the notion that a membrane defect exists in avian dystrophy. As neurogenic and vascular etiologies have also been proposed, we examined the characteristics of action potentials recorded in a novel in vivo preparation of the extensor digitorum communis muscle in 8-week-old normal and dystrophic chickens. To facilitate intracellular recording, dantrolene sodium was used to attenuate the muscle twitch. Results showed that although the resting membrane potential, action potential amplitude and the action potential maximum rate of rise were similar in normal and dystrophic cells, the action potential duration at half the maximum amplitude was increased in dystrophic cells. This observation has not been previously reported for dystrophic avian muscle and suggests that a defect in the sarcolemmal potassium conductance is an early change in dystrophic avian muscle.
在鸟类肌肉萎缩症模型中,电生理研究表明,体外培养的营养不良肌肉的动作电位特征发生了改变,这支持了鸟类肌肉萎缩症存在膜缺陷的观点。由于也有人提出神经源性和血管性病因,我们在8周龄正常和营养不良鸡的新型体内趾长伸肌制备物中检查了记录的动作电位特征。为便于细胞内记录,使用丹曲林钠减弱肌肉抽搐。结果表明,虽然正常细胞和营养不良细胞的静息膜电位、动作电位幅度和动作电位最大上升速率相似,但营养不良细胞中动作电位幅度减半时的动作电位持续时间增加。这一观察结果此前尚未在营养不良的鸟类肌肉中报道过,表明肌膜钾电导缺陷是营养不良鸟类肌肉的早期变化。