Ischemic Postconditioning Reduces NMDA Receptor Currents Through the Opening of the Mitochondrial Permeability Transition Pore and KATP Channel in Mouse Neurons

[1]  K. Shinzawa-Itoh,et al.  Purified F-ATP synthase forms a Ca2+-dependent high-conductance channel matching the mitochondrial permeability transition pore , 2019, Nature Communications.

[2]  I. Nakagawa,et al.  Ischemic postconditioning prevents surge of presynaptic glutamate release by activating mitochondrial ATP-dependent potassium channels in the mouse hippocampus , 2019, PLoS ONE.

[3]  M. Tymianski,et al.  Neurotransmitters in the mediation of cerebral ischemic injury , 2017, Neuropharmacology.

[4]  Yoshimasa Ito,et al.  Intravenous Administration of Cilostazol Nanoparticles Ameliorates Acute Ischemic Stroke in a Cerebral Ischemia/Reperfusion-Induced Injury Model , 2015, International journal of molecular sciences.

[5]  Ying Zhu,et al.  Prosurvival NMDA 2A receptor signaling mediates postconditioning neuroprotection in the hippocampus , 2015, Hippocampus.

[6]  L. Buck,et al.  Anoxia-mediated calcium release through the mitochondrial permeability transition pore silences NMDA receptor currents in turtle neurons , 2013, Journal of Experimental Biology.

[7]  D. Liebeskind,et al.  Ischemia-Reperfusion Injury in Stroke , 2013, Interventional Neurology.

[8]  C. Brenner,et al.  Physiological Roles of the Permeability Transition Pore , 2012, Circulation research.

[9]  L. Xiong,et al.  Inhibition of mitochondrial permeability transition pore opening contributes to the neuroprotective effects of ischemic postconditioning in rats , 2012, Brain Research.

[10]  M. Zoratti,et al.  Physiology of potassium channels in the inner membrane of mitochondria , 2011, Pflügers Archiv - European Journal of Physiology.

[11]  R. Bordet,et al.  Postconditioning in focal cerebral ischemia: Role of the mitochondrial ATP-dependent potassium channel , 2011, Brain Research.

[12]  M. Tymianski,et al.  Calcium, ischemia and excitotoxicity. , 2010, Cell calcium.

[13]  Heng Zhao.  Ischemic Postconditioning as a Novel Avenue to Protect against Brain Injury after Stroke , 2009, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[14]  Paolo Bernardi,et al.  Pathophysiology of mitochondrial volume homeostasis: potassium transport and permeability transition. , 2009, Biochimica et biophysica acta.

[15]  Z. Zuo,et al.  Postconditioning with Isoflurane Reduced Ischemia-induced Brain Injury in Rats , 2008, Anesthesiology.

[16]  B. Luo,et al.  Ischemic Postconditioning Protects Against Global Cerebral Ischemia/Reperfusion-Induced Injury in Rats , 2008, Stroke.

[17]  U. Brandt,et al.  K+-independent Actions of Diazoxide Question the Role of Inner Membrane KATP Channels in Mitochondrial Cytoprotective Signaling* , 2006, Journal of Biological Chemistry.

[18]  Y. Nakajima,et al.  Postconditioning, a Series of Brief Interruptions of Early Reperfusion, Prevents Neurologic Injury After Spinal Cord Ischemia , 2006, Annals of surgery.

[19]  R. Sapolsky,et al.  Interrupting Reperfusion as a Stroke Therapy: Ischemic Postconditioning Reduces Infarct Size after Focal Ischemia in Rats , 2006, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[20]  Q. Xia,et al.  Reactive oxygen species mediate the neuroprotection conferred by a mitochondrial ATP-sensitive potassium channel opener during ischemia in the rat hippocampal slice , 2005, Brain Research.

[21]  Quan-guang Zhang,et al.  Neuroprotective effects of preconditioning ischaemia on ischaemic brain injury through inhibition of mixed‐lineage kinase 3 via NMDA receptor‐mediated Akt1 activation , 2005, Journal of neurochemistry.

[22]  D. Busija,et al.  Diazoxide induces delayed pre‐conditioning in cultured rat cortical neurons , 2003, Journal of neurochemistry.

[23]  P. dos Santos,et al.  Mitochondrial potassium transport: the role of the mitochondrial ATP-sensitive K(+) channel in cardiac function and cardioprotection. , 2003, Biochimica et biophysica acta.

[24]  R. Guyton,et al.  Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning. , 2003, American journal of physiology. Heart and circulatory physiology.

[25]  A. Terzic,et al.  Targeting nucleotide-requiring enzymes: implications for diazoxide-induced cardioprotection. , 2003, American journal of physiology. Heart and circulatory physiology.

[26]  S. Javadov,et al.  The effects of ischaemic preconditioning, diazoxide and 5‐hydroxydecanoate on rat heart mitochondrial volume and respiration , 2002, The Journal of physiology.

[27]  J. Daut,et al.  KATP channel‐independent targets of diazoxide and 5‐hydroxydecanoate in the heart , 2002, The Journal of physiology.

[28]  I. Nakagawa,et al.  ATP-dependent potassium channel mediates neuroprotection by chemical preconditioning with 3-nitropropionic acid in gerbil hippocampus , 2002, Neuroscience Letters.

[29]  J. Downey,et al.  Opening of Mitochondrial KATP Channels Triggers the Preconditioned State by Generating Free Radicals , 2000, Circulation research.

[30]  P. Donohoe,et al.  Hypoxia-Induced Silencing of NMDA Receptors in Turtle Neurons , 2000, The Journal of Neuroscience.

[31]  D. Granger,et al.  Pathophysiology of ischaemia–reperfusion injury , 2000, The Journal of pathology.

[32]  B. Siesjö,et al.  Calcium in ischemic cell death. , 1998, Stroke.

[33]  K. Mikoshiba,et al.  ‘Ischemic tolerance’ phenomenon found in the brain , 1990, Brain Research.

[34]  H. Benveniste,et al.  Elevation of the Extracellular Concentrations of Glutamate and Aspartate in Rat Hippocampus During Transient Cerebral Ischemia Monitored by Intracerebral Microdialysis , 1984, Journal of neurochemistry.

[35]  R. Haworth,et al.  The Ca2+-induced membrane transition in mitochondria. I. The protective mechanisms. , 1979, Archives of biochemistry and biophysics.

[36]  R. Haworth,et al.  The Ca2+-induced membrane transition in mitochondria. II. Nature of the Ca2+ trigger site. , 1979, Archives of biochemistry and biophysics.

[37]  R. Haworth,et al.  The Ca2+-induced membrane transition in mitochondria. III. Transitional Ca2+ release. , 1979, Archives of biochemistry and biophysics.

[38]  G. Brierley.  The uptake and extrusion of monovalent cations by isolated heart mitochondria , 1976, Molecular and Cellular Biochemistry.