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10.3390/nu12092768 http://scihub22266oqcxt.onion/10.3390/nu12092768 32927908!7551965!32927908     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nutrients 2020 ; 12 (9): ä Nephropedia Template TP {{tp|p=32927908|t=2020. Inhibition of Mg(2+) Extrusion Attenuates Glutamate Excitotoxicity in Cultured Rat Hippocampal Neurons |pdf=|usr=}}{{32927908}} gab.com Text Inhibition of Mg(2+) Extrusion Attenuates Glutamate Excitotoxicity in Cultured Rat Hippocampal Neurons JO: Nutrients http://www.kidney.de/pget.php?&tw=1&pmid=32927908 #FOAvip Magnesium plays important roles in the nervous system. An increase in the Mg(2+) concentration in cerebrospinal fluid enhances neural functions, while Mg(2+) deficiency is implicated in neuronal diseases in the central nervous system. We have previously demonstrated that high concentrations of glutamate induce excitotoxicity and elicit a transient increase in the intracellular concentration of Mg(2+) due to the release of Mg(2+) from mitochondria, followed by a decrease to below steady-state levels. Since Mg(2+) deficiency is involved in neuronal diseases, this decrease presumably affects neuronal survival under excitotoxic conditions. However, the mechanism of the Mg(2+) decrease and its effect on the excitotoxicity process have not been elucidated. In this study, we demonstrated that inhibitors of Mg(2+) extrusion, quinidine and amiloride, attenuated glutamate excitotoxicity in cultured rat hippocampal neurons. A toxic concentration of glutamate induced both Mg(2+) release from mitochondria and Mg(2+) extrusion from cytosol, and both quinidine and amiloride suppressed only the extrusion. This resulted in the maintenance of a higher Mg(2+) concentration in the cytosol than under steady-state conditions during the ten-minute exposure to glutamate. These inhibitors also attenuated the glutamate-induced depression of cellular energy metabolism. Our data indicate the importance of Mg(2+) regulation in neuronal survival under excitotoxicity. Twit Text FOAVip Inhibition of Mg(2+) Extrusion Attenuates Glutamate Excitotoxicity in Cultured Rat Hippocampal Neurons ????Nutrients http://www.kidney.de/pget.php?&tw=1&pmid=32927908 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32927908 #FOAvip English Wikipedia <ref>{{Cite pmid|32927908}}</ref> Inhibition of Mg(2+) Extrusion Attenuates Glutamate Excitotoxicity in Cultured Rat Hippocampal Neurons #MMPMID32927908 Shindo Y; Yamanaka R; Hotta K; Oka K Nutrients 2020[Sep]; 12 (9): ä PMID32927908show ga Magnesium plays important roles in the nervous system. An increase in the Mg(2+) concentration in cerebrospinal fluid enhances neural functions, while Mg(2+) deficiency is implicated in neuronal diseases in the central nervous system. We have previously demonstrated that high concentrations of glutamate induce excitotoxicity and elicit a transient increase in the intracellular concentration of Mg(2+) due to the release of Mg(2+) from mitochondria, followed by a decrease to below steady-state levels. Since Mg(2+) deficiency is involved in neuronal diseases, this decrease presumably affects neuronal survival under excitotoxic conditions. However, the mechanism of the Mg(2+) decrease and its effect on the excitotoxicity process have not been elucidated. In this study, we demonstrated that inhibitors of Mg(2+) extrusion, quinidine and amiloride, attenuated glutamate excitotoxicity in cultured rat hippocampal neurons. A toxic concentration of glutamate induced both Mg(2+) release from mitochondria and Mg(2+) extrusion from cytosol, and both quinidine and amiloride suppressed only the extrusion. This resulted in the maintenance of a higher Mg(2+) concentration in the cytosol than under steady-state conditions during the ten-minute exposure to glutamate. These inhibitors also attenuated the glutamate-induced depression of cellular energy metabolism. Our data indicate the importance of Mg(2+) regulation in neuronal survival under excitotoxicity. |Amiloride/*pharmacology[MESH] |Animals[MESH] |Cells, Cultured[MESH] |Cytosol/metabolism[MESH] |Glutamic Acid/*toxicity[MESH] |Hippocampus/cytology[MESH] |Magnesium/*physiology[MESH] |Mitochondria/metabolism[MESH] |Neurons/*drug effects[MESH] |Quinidine/*pharmacology[MESH]Inhibition of Mg(2+) Extrusion Attenuates Glutamate Excitotoxicity in (epmc).pdf DeepDyve Pubget Overpricing