Mild hypothermia protects rat hippocampal CA1 neurons from irreversible membrane dysfunction induced by experimental ischemia
Mild hypothermia protects rat hippocampal CA1 neurons from irreversible membrane dysfunction induced by experimental ischemia
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DOI：
10.1016/s0168-0102(97)00110-7
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发表时间：
1998-01-01
影响因子：
2.9
通讯作者：
Higashi, H
中科院分区：
文献类型：
--
作者：
Onitsuka, M;Mihara, S;Higashi, H
为了观察低温对实验性缺血（缺氧缺糖）引起的膜电位变化的影响，在大鼠海马脑片上对单个CA_1锥体神经元进行了细胞内记录。缺血介质的应用引起膜电位的不可逆变化，包括初始超极化，然后缓慢去极化和快速去极化。在35 ° C和37 ° C的温度下，一旦发生快速去极化，再给予氧和葡萄糖不能恢复膜电位，这种状态被称为不可逆的膜功能障碍。当温度降低到27摄氏度和33摄氏度之间时，75%的神经元的膜电位恢复到对照静息膜电位。快速除极的潜伏期、振幅和最大斜率的温度系数（Q（10））分别为2.5、1.4和2.9。II的结论是，在缺血引起的膜功能障碍的临界神经保护温度被发现是33摄氏度在单个CA1神经元在体外。(C)1998爱思唯尔科学爱尔兰有限公司保留所有权利。
In order to examine the effects of hypothermia on the changes in membrane potential induced by experimental ischemia (deprivation of oxygen and glucose), intracellular recordings were made from single CA1 pyramidal neurons in slice preparations of rat hippocampus. Application of ischemic medium caused irreversible changes in membrane potential consisting of an initial hyperpolarization, then a slow depolarization and a rapid depolarization. Al temperatures of 35 degrees C and 37 degrees C, once the rapid depolarization occurred, readministration of oxygen and glucose failed to restore the membrane potential, a state referred to as irreversible membrane dysfunction. When the temperature was lowered to between 27 degrees C and 33 degrees C, the membrane potential returned to the control resting membrane potential in 75% of the neurons. The temperature coefficients (Q(10)) of the latency, the amplitude, and the maximal slope of the rapid depolarization were 2.5, 1.4 and 2.9, respectively. II is concluded that the critical neuroprotective temperature in ischemia-induced membrane dysfunction is found to be 33 degrees C in single CA1 neurons in vitro. (C) 1998 Elsevier Science Ireland Ltd. All rights reserved.