NMDA antagonists prevent hypothermic injury and death of mammalian spinal neurons.
NMDA antagonists prevent hypothermic injury and death of mammalian spinal neurons.
复制标题
NMDA 拮抗剂可防止哺乳动物脊髓神经元的低温损伤和死亡。
DOI：
10.1089/neu.1990.7.229
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发表时间：
1990
影响因子：
4.2
通讯作者：
Gross,GW
中科院分区：
文献类型：
--
作者：
Lucas,JH;Wang,GF;Gross,GW
在低于 17°C 的温度下长时间（2-6 小时）冷却分离的小鼠脊髓单层培养物会导致神经元核周和树突明显肿胀。培养物中肿胀神经元的数量随着温度的降低而增加，并且在 7°C–10°C 时所有神经元都肿胀。将培养物重新加热至 37°C 后，大多数肿胀的神经元死亡（10°C 时高达 74%）。神经胶质细胞不受影响。在将温度降至 10°C 之前，向脊髓培养物中添加 NMDA 拮抗剂 d-2-氨基-5-磷酸戊酸 (DAPV，100 μM)、氯胺酮 (100 μM) 和二苯并环庚烯亚胺 (MK801，10 μM) 可最大程度地减少树突体肿胀，并将神经元死亡率从 74% 降低至 10%。这些数据显示一些神经元对非冰冻低温具有惊人的敏感性，并表明 NMDA 受体直接参与与低温相关的神经元死亡。
Prolonged (2–6 h) cooling of monolayer cultures of dissociated murine spinal cord at temperatures below 17°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°C–10°C all of the neurons were swollen. On rewarming the cultures to 37°C, the majority of the swollen neurons died (up to 74% at 10°C). Glial cells were not affected. Addition of the NMDA antagonistsd-2-amino-5-phosphonovalerate (DAPV, 100 μM), ketamine (100 μM), and dibenzocyclohepteneimine (MK801, 10 μM) to spinal cord cultures before lowering the temperature to 10°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.