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γ-氨基丁酸能神经元和胆碱能神经元对短暂性脑缺血的反应。

The response of GABAergic and cholinergic neurons to transient cerebral ischemia.

作者信息

Francis A, Pulsinelli W

出版信息

Brain Res. 1982 Jul 15;243(2):271-8. doi: 10.1016/0006-8993(82)90250-5.

Abstract

The vulnerability of striatal and hippocampal neurons to ischemia was studied by measuring the activity of neurotransmitter-related enzymes after transient forebrain ischemia in rats. Activities of glutamic acid decarboxylase (GAD) and choline acetyltransferase (CAT) were measured 6 h to 8 days after 20, 30 or 40 min of forebrain ischemia, as markers for GABAergic and cholinergic neurons respectively. Transient forebrain ischemia resulted in depression of striatal GAD activity while striatal CAT and hippocampal GAD activities were unaffected. Striatal GAD activity progressively decreased during the first 24 h postischemia and remained depressed 5--8 days later, suggesting irreversible damage to this population of neurons. The stability of striatal CAT and hippocampal GAD activity indicates that these cells were resistant to the present ischemic conditions.

摘要

通过测量大鼠短暂性前脑缺血后神经递质相关酶的活性,研究纹状体和海马神经元对缺血的易损性。分别在20、30或40分钟前脑缺血后6小时至8天测量谷氨酸脱羧酶(GAD)和胆碱乙酰转移酶(CAT)的活性,作为GABA能和胆碱能神经元的标志物。短暂性前脑缺血导致纹状体GAD活性降低,而纹状体CAT和海马GAD活性未受影响。纹状体GAD活性在缺血后最初24小时内逐渐降低,并在5-8天后仍保持降低,提示这群神经元发生了不可逆损伤。纹状体CAT和海马GAD活性的稳定性表明这些细胞对当前的缺血条件具有抗性。

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