Lucas J H, Wang G F, Gross G W
Center for Network Neuroscience, University of North Texas, Denton.
J Neurotrauma. 1990 Winter;7(4):229-36. doi: 10.1089/neu.1990.7.229.
Prolonged (2-6 h) cooling of monolayer cultures of dissociated murine spinal cord at temperatures below 17 degrees C caused pronounced swelling of neuronal perikarya and dendrites. The numbers of swollen neurons in a culture increased as the temperature was reduced, and at 7 degrees C-10 degrees C all of the neurons were swollen. On rewarming the cultures to 37 degrees C, the majority of the swollen neurons died (up to 74% at 10 degrees C). Glial cells were not affected. Addition of the NMDA antagonists D-2-amino-5-phosphonovalerate (DAPV, 100 microM), ketamine (100 microM), and dibenzocyclohepteneimine (MK801, 10 microM) to spinal cord cultures before lowering the temperature to 10 degrees C minimized the dendrosomatic swelling and reduced neuronal mortality from 74% to 10%. These data show a surprising sensitivity of some neurons to nonfreezing low temperatures and suggest direct involvement of the NMDA receptor in hypothermia-related neuronal death.
将离体小鼠脊髓单层培养物在低于17摄氏度的温度下长时间（2 - 6小时）冷却，会导致神经元胞体和树突明显肿胀。培养物中肿胀神经元的数量随温度降低而增加，在7摄氏度至10摄氏度时所有神经元都发生肿胀。将培养物复温至37摄氏度时，大多数肿胀神经元死亡（在10摄氏度时高达74%）。胶质细胞未受影响。在将温度降至10摄氏度之前，向脊髓培养物中添加NMDA拮抗剂D - 2 - 氨基 - 5 - 膦酰戊酸（DAPV，100微摩尔）、氯胺酮（100微摩尔）和二苯并环庚烯亚胺（MK801，10微摩尔），可使树突体肿胀最小化，并将神经元死亡率从74%降至10%。这些数据显示某些神经元对非冷冻低温具有惊人的敏感性，并表明NMDA受体直接参与了与体温过低相关的神经元死亡。
