Pushkarev Iu P
Probl Endokrinol (Mosk). 1978 Mar-Apr;24(2):77-81.
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.
对病程较短（1 - 5周）但已出现症状（血糖水平为150至350毫克%）的四氧嘧啶糖尿病大鼠的离体骨骼肌进行了微电极细胞内记录突触后电位的实验。在这种情况下，神经肌肉突触传递的显著紊乱完全是由突触前终末兴奋性能力的降低所引起的。观察到终板微电位（PEP）频率降低，以及PEP量子成分减少。在测定介质转化的动态特性时发现，介质合成强度明显降低，而乙酰胆碱分泌分数无明显抑制。这是糖尿病动物中可供使用的介质部分缺乏的原因。
