Pushkarev Iu P
Biull Eksp Biol Med. 1979 Apr;87(4):305-8.
Insulin-induced hypoglycemia caused depression of rhythmic monosynaptic EPSP motoneurons of the lumbar cord in acute experiments on narcotized and spinal cats. It was demonstrated that growing depression of monosynaptic transmission was associated with the exhaustion of mediator operative fraction and not with any pre- or postsynaptic delay or inhibition over a period of initial hypoglycemia when the sugar content in the blood fell to the level of 50--60 mg%. The function disturbance of postsynaptic formations of monosynaptic reflex arc of spinal cord occured in more advanced hypoglycemia.
在对麻醉猫和脊髓猫进行的急性实验中，胰岛素诱导的低血糖导致腰髓节律性单突触兴奋性突触后电位运动神经元受到抑制。结果表明，单突触传递的逐渐抑制与介质活性部分的耗竭有关，而与低血糖初期（此时血糖水平降至50 - 60毫克%）期间的任何突触前或突触后延迟或抑制无关。脊髓单突触反射弧突触后结构的功能障碍发生在更严重的低血糖阶段。
