Magnesium sulfate protects against the bioenergetic consequences of chronic glutamate receptor stimulation.
Magnesium sulfate protects against the bioenergetic consequences of chronic glutamate receptor stimulation.
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DOI：
10.1371/journal.pone.0079982
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Polster BM
中科院分区：
文献类型：
--
作者：
Clerc P;Young CA;Bordt EA;Grigore AM;Fiskum G;Polster BM
细胞外谷氨酸在脑缺血或创伤后升高，并有助于神经元损伤。我们测试的假设，硫酸镁（MgSO4，3 mM）保护兴奋毒性谷氨酸暴露引起的代谢衰竭。在已经含有生理浓度Mg2+（1 mM）的培养基中处理的大鼠皮质神经元制备物可以根据其对谷氨酸（100 µM）的反应进行分离。I型制剂的反应是耗氧率（OCR）降低或短暂增加。II型神经元在OCR中以>50%的刺激响应，表明对增加的能量需求的稳健响应，而没有立即的毒性。用MgSO4预处理改善了对谷氨酸的初始生物能反应，并改善了随后的备用呼吸能力的丧失，测量后加入解偶联剂FCCP，在I型但不是II型神经元。I型神经元中的备用呼吸能力也通过在没有谷氨酸处理的情况下与MgSO 4或NMDA受体拮抗剂MK 801孵育而得到改善。这一发现表明，I型和II型制剂之间的主要差异是内源性谷氨酸受体活性的量。在暴露于兴奋性毒性（100 µM）谷氨酸之前，将II型神经元与5 µM谷氨酸孵育，重现了I型表型。MgSO4可防止兴奋毒性谷氨酸诱导的神经元ATP下降，无论是否预先暴露于5 µM谷氨酸。结果表明，MgSO4保护慢性中度谷氨酸受体刺激，并保留细胞ATP兴奋毒性谷氨酸治疗后。
Extracellular glutamate is elevated following brain ischemia or trauma and contributes to neuronal injury. We tested the hypothesis that magnesium sulfate (MgSO4, 3 mM) protects against metabolic failure caused by excitotoxic glutamate exposure. Rat cortical neuron preparations treated in medium already containing a physiological concentration of Mg2+ (1 mM) could be segregated based on their response to glutamate (100 µM). Type I preparations responded with a decrease or small transient increase in oxygen consumption rate (OCR). Type II neurons responded with >50% stimulation in OCR, indicating a robust response to increased energy demand without immediate toxicity. Pre-treatment with MgSO4 improved the initial bioenergetic response to glutamate and ameliorated subsequent loss of spare respiratory capacity, measured following addition of the uncoupler FCCP, in Type I but not Type II neurons. Spare respiratory capacity in Type I neurons was also improved by incubation with MgSO4 or NMDA receptor antagonist MK801 in the absence of glutamate treatment. This finding indicates that the major difference between Type I and Type II preparations is the amount of endogenous glutamate receptor activity. Incubation of Type II neurons with 5 µM glutamate prior to excitotoxic (100 µM) glutamate exposure recapitulated a Type I phenotype. MgSO4 protected against an excitotoxic glutamate-induced drop in neuronal ATP both with and without prior 5 µM glutamate exposure. Results indicate that MgSO4 protects against chronic moderate glutamate receptor stimulation and preserves cellular ATP following treatment with excitotoxic glutamate.
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影响因子：
4
作者：
Kovac S;Domijan AM;Walker MC;Abramov AY
通讯作者：
Abramov AY
影响因子：
6
作者：
Lampl, Y;Geva, D;Sarova-Pinhas, I
通讯作者：
Sarova-Pinhas, I
DOI：
10.3109/00365519509075397
发表时间：
1995-12-01
影响因子：
2.1
作者：
Memon, ZI;Altura, BT;Altura, BM
通讯作者：
Altura, BM
影响因子：
5.3
作者：
Yakovlev, AG;Ota, K;Faden, AI
通讯作者：
Faden, AI
急性谷氨酸兴奋性毒性中细胞质钙蛋白酶激活和钙失调的实时可视化。
影响因子：
4.7
作者：
Gerencser AA;Mark KA;Hubbard AE;Divakaruni AS;Mehrabian Z;Nicholls DG;Polster BM
通讯作者：
Polster BM