Kazan State Medical University, Ministry of Health of the Russian Federation, , Kazan, Republic of Tatarstan, Russia.
Bull Exp Biol Med. 2024 Aug;177(4):449-453. doi: 10.1007/s10517-024-06206-9. Epub 2024 Sep 12.
In experiments on the motor nerve endings of the diaphragm of transgenic FUS mice with a model of amyotrophic lateral sclerosis at the pre-symptomatic stage of the disease, the processes of transmitter release and endocytosis of synaptic vesicles were studied. In FUS mice, the intensity of transmitter release during high-frequency stimulation of the motor nerve (50 imp/sec) was lowered. At the same duration of stimulation, the loading of fluorescent dye FM1-43 was lower in FUS mice. However, at the time of stimulation, during which an equal number of quanta are released in wild-type and FUS mice, no differences in the intensity of dye loading were found. Thus, endocytosis is not the key factor in the mechanism of synaptic dysfunction in FUS mice at the pre-symptomatic stage.
在疾病前症状阶段肌萎缩侧索硬化症模型的转基因 FUS 小鼠膈肌运动神经末梢的实验中，研究了递质释放和突触囊泡内吞的过程。在 FUS 小鼠中，运动神经高频刺激（50 次/秒）时递质释放的强度降低。在相同的刺激持续时间内，FUS 小鼠中荧光染料 FM1-43 的加载量较低。然而，在刺激期间，在野生型和 FUS 小鼠中释放相同数量的量子时，发现染料加载强度没有差异。因此，内吞作用不是 FUS 小鼠在疾病前症状阶段突触功能障碍机制中的关键因素。
