Lactate produced by glycogenolysis in astrocytes regulates memory processing.
Lactate produced by glycogenolysis in astrocytes regulates memory processing.
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DOI：
10.1371/journal.pone.0028427
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发表时间：
2011
期刊：
影响因子：
3.7
通讯作者：
Gold PE
中科院分区：
文献类型：
--
作者：
Newman LA;Korol DL;Gold PE
当全身或中枢给药时，葡萄糖是记忆过程的有效增强剂。在记忆测试过程中，测量大鼠海马细胞外液中的葡萄糖水平显示，这些水平是动态的，响应于记忆任务和负荷而降低;外源性葡萄糖阻断这些降低并增强记忆。目前的实验测试的假设，葡萄糖增强记忆是由糖原储存，然后代谢成乳酸的星形胶质细胞，提供乳酸作为能量底物的神经元介导的。使用敏感的生物探针测量1秒样品中的脑葡萄糖和乳酸水平。当大鼠进行空间工作记忆任务时，细胞外葡萄糖减少，乳酸增加。海马内注入乳酸盐增强了这项任务的记忆。此外，星形胶质细胞糖原分解的药理学抑制损害记忆，这种损害被逆转的乳酸或葡萄糖，这两者都可以提供乳酸的神经元在糖原分解的情况下，管理。药理学阻断负责乳酸摄取进入神经元的单羧酸转运蛋白也损害记忆，这种损害不能被葡萄糖或乳酸逆转。这些发现支持了星形胶质细胞通过控制乳酸的供应来支持神经元功能来调节记忆形成的观点。
When administered either systemically or centrally, glucose is a potent enhancer of memory processes. Measures of glucose levels in extracellular fluid in the rat hippocampus during memory tests reveal that these levels are dynamic, decreasing in response to memory tasks and loads; exogenous glucose blocks these decreases and enhances memory. The present experiments test the hypothesis that glucose enhancement of memory is mediated by glycogen storage and then metabolism to lactate in astrocytes, which provide lactate to neurons as an energy substrate. Sensitive bioprobes were used to measure brain glucose and lactate levels in 1-sec samples. Extracellular glucose decreased and lactate increased while rats performed a spatial working memory task. Intrahippocampal infusions of lactate enhanced memory in this task. In addition, pharmacological inhibition of astrocytic glycogenolysis impaired memory and this impairment was reversed by administration of lactate or glucose, both of which can provide lactate to neurons in the absence of glycogenolysis. Pharmacological block of the monocarboxylate transporter responsible for lactate uptake into neurons also impaired memory and this impairment was not reversed by either glucose or lactate. These findings support the view that astrocytes regulate memory formation by controlling the provision of lactate to support neuronal functions.
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影响因子：
2.9
作者：
Donohoe, RT;Benton, D
通讯作者：
Benton, D
影响因子：
2.6
作者：
BENTON, D;OWENS, DS;PARKER, PY
通讯作者：
PARKER, PY
DOI：
10.1016/0165-3806(91)90171-e
发表时间：
1991-10-21
期刊：
DEVELOPMENTAL BRAIN RESEARCH
影响因子：
--
作者：
BRUNJES, PC;CAGGIANO, AO;STEWART, JS
通讯作者：
STEWART, JS
影响因子：
2.9
作者：
Benton, David;Maconie, Alys;Williams, Claire
通讯作者：
Williams, Claire
DOI：
10.1152/ajpendo.2000.278.4.e571
发表时间：
2000-04-01
影响因子：
5.1
作者：
Dubouchaud, H;Butterfield, GE;Brooks, GA
通讯作者：
Brooks, GA