TAURINE IMPROVES THE RECOVERY OF NEURONAL FUNCTION FOLLOWING CEREBRAL HYPOXIA - AN INVITRO STUDY
TAURINE IMPROVES THE RECOVERY OF NEURONAL FUNCTION FOLLOWING CEREBRAL HYPOXIA - AN INVITRO STUDY
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DOI：
10.1016/0024-3205(87)90098-1
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发表时间：
1987-05-25
期刊：
影响因子：
6.1
通讯作者：
RIGOR, BM
中科院分区：
文献类型：
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作者：
SCHURR, A;TSENG, MT;RIGOR, BM
在本研究中，大鼠海马脑片被用来评估与氨基酸牛磺酸的预处理对他们的能力恢复突触功能后，标准化的缺氧损伤的影响。缺氧10分钟后，47%的所有对照（未处理）切片表现出突触功能的恢复（顺向诱发的CA 1群体尖峰）。用0.5，1.0或2.0 mM牛磺酸预处理的切片，63，88和97%从相同的缺氧损伤中恢复。这种剂量依赖性保护作用是双相的，因为5.0 mM牛磺酸不产生保护作用。当缺氧延长到15分钟，只有20%的未处理的切片恢复，而88%的切片与1.0 mM牛磺酸治疗恢复其人口尖峰。同样的预处理衰减下降的人口尖峰幅度后，Ca2+耗尽。我们推测，牛磺酸通过衰减跨神经元膜的Ca 2+运动在内源性抗缺氧机制中起着重要作用。
Rat hippocampal slices were used in the present study to assess the effect of a pretreatment with the amino acid taurine on their ability to recover synaptic function following a standardized hypoxic insult. After 10 min hypoxia, 47% of all control (untreated) slices exhibited recovery of synaptic function (orthodromically evoked CA1 population spike). Of slices pretreated with 0.5, 1.0 or 2.0 mM taurine, 63, 88 and 97% recovered from the same hypoxic insult. This dose-dependent protective effect was biphasic, as 5.0 mM taurine produced no protection. When hypoxia was extended to 15 min, only 20% of the untreated slices recovered, while 88% of slices treated with 1.0 mM taurine recovered their population spike. The same pretreatment attenuated the fall in the population spike amplitude upon Ca2+ depletion. We hypothesize that taurine plays an important role in an endogenous antihypoxic mechanism through the attenuation of Ca2+ movement across the neuronal membrane.