低血糖及缺氧恢复对突触体代谢的体外效应。
The effects in vitro of hypoglycaemia and recovery from anoxia on synaptosomal metabolism.
作者信息
Harvey S A, Booth R F, Clark J B
出版信息
Biochem J. 1982 Sep 15;206(3):433-9. doi: 10.1042/bj2060433.
Abstract
Synaptosomes from several regions of the rat brain were found to exhibit half-maximal rates of 14CO2 output and [14C]acetylcholine synthesis from D-[U-14C]glucose at glucose concentrations approx. 50-fold lower than those required by the brain in situ. However, synaptosomal acetylcholine synthesis was found not to be directly proportional to substrate oxidation as measured by 14CO2 output. When synaptosomes had been exposed to anoxia in vitro, their metabolic indices (14CO2 and [14C]acetylcholine synthesis, and adenine nucleotide levels) were found not to be significantly different from control aerobic values, unless they had been subjected to veratridine depolarization. This is in accord with previous findings that neither the absolute metabolic rates nor the vulnerability to hypoxic damage exhibited by brain in situ is reflected by brain slices in vitro, unless these are stimulated by depolarization. The use of synaptosomes as a model for synaptic damage in vivo is discussed.
摘要
研究发现，来自大鼠脑多个区域的突触体，在葡萄糖浓度约比脑原位所需浓度低50倍的情况下，从D-[U-¹⁴C]葡萄糖产生¹⁴CO₂输出和[¹⁴C]乙酰胆碱合成的半最大速率。然而，发现突触体乙酰胆碱合成与通过¹⁴CO₂输出测量的底物氧化并不直接成比例。当突触体在体外暴露于缺氧状态时，除非它们经历了藜芦碱去极化，否则其代谢指标（¹⁴CO₂和[¹⁴C]乙酰胆碱合成以及腺嘌呤核苷酸水平）与对照需氧值没有显著差异。这与先前的研究结果一致，即除非通过去极化刺激，否则体外脑切片无法反映脑原位的绝对代谢率和对缺氧损伤的易感性。本文讨论了使用突触体作为体内突触损伤模型的情况。
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