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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Energy transfer from astrocytes to axons: the role of CNS glycogen.
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Energy transfer from astrocytes to axons: the role of CNS glycogen.

机译：从星形胶质细胞到轴突的能量转移：中枢神经系统糖原的作用。

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摘要

We tested the hypothesis that astrocytic glycogen supports axon function under both pathological and physiological conditions. Functional activity of the rat (RON) or mouse optic nerve (MON), representative central white matter tracts, was assessed electrophysiologically as the area under the supramaximal compound action potential (CAP). During aglycaemia the CAP area of rodent optic nerve persisted for up to 30 min, after which the CAP rapidly failed. Glycogen content measured biochemically during the aglycaemic insult fell with a time course compatible with its rapid degradation in the absence of glucose. Pharmacological up-regulation of glycogen content prior to the aglycaemic insult with incubation in hyperglycaemic ambient glucose delayed CAP failure, whereas down-regulation of glycogen content induced by nor-adrenaline accelerated CAP failure. Inhibiting lactate transfer between astrocytes and axons during aglycaemia, where glycogen is the only utilisable energy reserve, resulted in accelerated CAP failure, implying that glycogen-derived lactate supports function when exogenous energy metabolites are withdrawn. Under normoglycaemic conditions glycogen content decreased during high frequency axon discharge, although CAP function was fully maintained. Both prior depletion of glycogen content, or blocking axonal lactate uptake rendered nerves incapable of fully supporting CAP function during high frequency firing in the presence of normoglycaemic glucose. These results indicated that during aglycaemia and increased metabolic demand, astrocytic glycogen was degraded to form lactate, which was used as a supplemental energy source when ambient normoglycaemic glucose was incapable of meeting immediate tissue energy demands.
机译：我们检验了在病理和生理条件下星形细胞糖原均支持轴突功能的假说。将大鼠（RON）或小鼠视神经（MON）（代表中央白质束）的功能活性通过电生理学评估为超最大复合动作电位（CAP）下的面积。在无糖期间，啮齿动物视神经的CAP区域持续长达30分钟，此后CAP迅速失效。在无糖事件中，通过生物化学方法测得的糖原含量随时间变化而下降，这与其在没有葡萄糖时的快速降解相吻合。在高血糖环境葡萄糖中进行无糖血症孵育之前，糖原含量的药理上调延迟了CAP衰竭，而去甲肾上腺素诱导的糖原含量下调则加速了CAP衰竭。糖原是唯一可利用的能量储备，在无糖血症期间抑制星形胶质细胞和轴突之间的乳酸盐转移会导致CAP加速衰竭，这意味着当提取外源性能量代谢产物时，糖原衍生的乳酸盐会支持功能。在正常血糖条件下，尽管完全维持了CAP功能，但糖原含量在高频轴突放电过程中降低了。在存在正常血糖的葡萄糖的情况下，高频放电期间，既往糖原含量的耗尽或阻断轴突乳酸盐的摄取都使神经无法完全支持CAP功能。这些结果表明，在无糖血症和新陈代谢需求增加期间，星形细胞糖原被降解形成乳酸，当周围的正常血糖不能满足组织的即时能量需求时，乳酸被用作补充能源。

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