[Mechanisms of neuromuscular transmission disorder in rats with alloxan diabetes].
A microelectrode intracellular leading off of the postsynaptic potentials of isolated skeletal muscles was carried out in rats with alloxan diabetes of short duration (1--5 weeks), but manifest (blood sugar level from 150 to 350 mg%). A significant disturbance of the neuro-muscular synaptic transmission in this case was wholly caused by the reduction of the excitatory capacity of the presynaptic terminals. There was seen a reduction of the frequency of the miniature potentials of end plates (PEP), and a reduction of quant PEP composition. A distinct reduction of the intensity of the mediator synthesis, without any significant suppression of the fractional acetylcholine secretion was revealed in determination of the dynamic characteristics of the mediator transformations. This served as the cause of a deficiency of the fraction of a mediator ready for use in the animals suffering from diabetes.
D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000150:complications* / Q000503:physiopathology; D004558:Electric Stimulation; D005071:Evoked Potentials; D005260:Female; D009468:Neuromuscular Diseases / Q000209:etiology* / Q000503:physiopathology; D009469:Neuromuscular Junction / Q000503:physiopathology; D051381:Rats; D009435:Synaptic Transmission; D013997:Time Factors
Mekhanizm narusheniia nervno-myshechnoĭ peredachi u krys s alloksanovym diabetom.