Monocarboxylates and glucose utilization as energy substrates in rat brain slices under selective glial poisoning -: a 31P NMR study
Monocarboxylates and glucose utilization as energy substrates in rat brain slices under selective glial poisoning -: a 31P NMR study
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DOI：
10.1023/a:1022461118479
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发表时间：
2003-02-01
影响因子：
4.3
通讯作者：
Yokoi, I
中科院分区：
文献类型：
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作者：
Kitano, T;Nisimaru, N;Yokoi, I
我们利用P-31核磁共振研究了葡萄糖、乳酸和丙酮酸等多种能量底物对高k +刺激后大鼠脑切片高能量磷酸盐水平恢复的影响。研究发现，乳酸、丙酮酸和葡萄糖对人工脑脊液（ACSF）高k +刺激（60 mM, 8 min）后磷酸肌酸（PCr）水平恢复的支持作用几乎相同。在碘乙酸（IAA）和氟柠檬酸（FC）预处理的切片中，由于葡萄糖无法被利用，高k +刺激后含有乳酸的ACSF中PCr水平的恢复完全被取消，含有丙酮酸的ACSF中PCr的恢复不受影响。这些结果表明，如果没有神经胶质的支持，神经元本身可以利用丙酮酸盐作为外源能量底物，而不是乳酸盐。在完整的大脑中，葡萄糖可能在神经胶质细胞中代谢成丙酮酸，然后作为能量底物转运到神经元。这些提示星形胶质细胞-神经元丙酮酸穿梭机制在体内的大脑能量代谢。我们还研究了缺血预处理对fc预处理切片的影响，结果表明，高k +刺激后，含有乳酸的ACSF中PCr水平大幅恢复。这表明在预处理后，如缺血，神经元本身获得了利用乳酸作为能量底物的能力。
We have investigated effects of various energy substrates including glucose, lactate and pyruvate on the recovery of the high energy phosphate levels after high-K+ stimulation in rat brain slices by using P-31 NMR. It was found that lactate, pyruvate and glucose almost equally supported the recovery of phosphocreatine (PCr) levels after high-K+ stimulation (60 mM, 8 min) in artificial cerebrospinal fluid (ACSF). In iodoacetic acid (IAA) and fluorocitrate (FC)-pretreated slices, whereas glucose was unable to be utilized, the recovery of the PCr level after high-K+ stimulation in ACSF containing lactate was completely abolished, the recovery of the PCr in ACSF containing pyruvate was unaffected. These results indicate that neurons themselves can utilize pyruvate as an exogenous energy substrate, but not lactate, without glial support. In intact brain, glucose may be metabolized to pyruvate in glial cells and then transported to neurons as an energy substrate. These suggest an astrocyte-neuron pyruvate shuttle mechanism of the brain energy metabolism in vivo.We also investigated the effect of ischemic-preconditioning in FC-pretreated slices, which showed that the PCr levels recovered substantially in ACSF containing lactate after high-K+ stimulation. This indicates that after the preconditioning, such as ischemia, neurons themselves acquired the ability to utilize lactate as an energy substrate.