Chikin A V, Urazaev A Kh, Volkov E M, Poletaev G I, Khamitov Kh S
Neirofiziologiia. 1987;19(6):759-66.
A decrease in the resting membrane potential, an increase in the input resistance, appearance of the anode breakdown and tetrodotoxin-resistant action potentials and extrajunctional acetylcholine sensitivity following denervation were revealed in surviving rat diaphragm muscle fibres. Addition of beta-endorphin (1.10(-8) M) to the culture medium prevented on increase in the input resistance and reduced a degree of the extrajunctional acetylcholine sensitivity, but did not inhibit the appearance of the anode breakdown and tetrodotoxin-resistant action potentials. Naloxone (1.25.10(-6) M) did not avert the effect of beta-endorphin, more over it exerted a beta-endorphin-like effect on the denervated muscle fibres. It is suggested that beta-endorphin can be the factor which is responsible for the neurotrophic control of passive electrical properties of the muscle fibre membrane and neurotrophic regulation of the membrane sensitivity to acetylcholine.
在存活的大鼠膈肌纤维中发现,去神经支配后静息膜电位降低、输入电阻增加、出现阳极崩解以及对河豚毒素耐受的动作电位和接头外乙酰胆碱敏感性增加。向培养基中添加β-内啡肽(1×10⁻⁸ M)可防止输入电阻增加,并降低接头外乙酰胆碱敏感性的程度,但不抑制阳极崩解和对河豚毒素耐受的动作电位的出现。纳洛酮(1.25×10⁻⁶ M)不能避免β-内啡肽的作用,此外,它对去神经支配的肌肉纤维产生类似β-内啡肽的作用。提示β-内啡肽可能是负责对肌纤维膜的被动电特性进行神经营养控制以及对膜对乙酰胆碱的敏感性进行神经营养调节的因素。