MK801 decreases glutamate release and oxidative metabolism during hypoglycemic coma in piglets.

[1]  M. Moskowitz,et al.  Pathobiology of ischaemic stroke: an integrated view , 1999, Trends in Neurosciences.

[2]  R. Ichord,et al.  Brain O2 consumption and glutamate release during hypoglycemic coma in piglets are temperature sensitive. , 1999, American journal of physiology. Heart and circulatory physiology.

[3]  G. Brown,et al.  Nitric Oxide Causes Glutamate Release from Brain Synaptosomes , 1998, Journal of neurochemistry.

[4]  D. Nicholls,et al.  Exocytotic and Nonexocytotic Modes of Glutamate Release from Cultured Cerebellar Granule Cells During Chemical Ischaemia , 1998, Journal of neurochemistry.

[5]  A. Wenzel,et al.  Synapse‐specific localization of NMDA and GABAA receptor subunits revealed by antigen‐retrieval immunohistochemistry , 1998, The Journal of comparative neurology.

[6]  H. Nukui,et al.  The time course of glucose metabolism in rat cerebral ischemia with middle cerebral artery occlusion-reperfusion model and the effect of MK-801. , 1996, Neurological research.

[7]  J. Garthwaite,et al.  Vicious Cycle Involving Na+ Channels, Glutamate Release, and NMDA Receptors Mediates Delayed Neurodegeneration through Nitric Oxide Formation , 1996, The Journal of Neuroscience.

[8]  M. Johnston,et al.  The ontogeny of glutamate receptors in rat barrel field cortex. , 1995, Brain research. Developmental brain research.

[9]  P. Magistretti,et al.  Glutamate uptake into astrocytes stimulates aerobic glycolysis: a mechanism coupling neuronal activity to glucose utilization. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[10]  M. Kuhar,et al.  Nitric oxide inhibits 3H‐glutamate transport in synaptosomes , 1994, Synapse.

[11]  M. Plotkine,et al.  Competitive NMDA receptor blockers reduce striatal glutamate accumulation in ischaemia. , 1994, Neuroreport.

[12]  R. Ichord,et al.  Nitric oxide synthase inhibition attenuates hypoglycemic cerebral hyperemia in piglets. , 1994, The American journal of physiology.

[13]  M. Tsuji,et al.  Effects of MK-801 and NBQX on Acute Recovery of Piglet Cerebral Metabolism after Hypothermic Circulatory Arrest , 1994, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[14]  R. Traystman,et al.  MK-801 does not prevent impaired cerebrovascular reactivity to CO2 during hypoglycemia in piglets. , 1993, The American journal of physiology.

[15]  J. Korf,et al.  Glutamate dehydrogenase improves binding of [3H]CGP39653 to NMDA receptors in the autoradiographic assay , 1993, Journal of Neuroscience Methods.

[16]  J. Coyle,et al.  The regional vulnerability to hypoglycemia-induced neurotoxicity in organotypic hippocampal culture: protection by early tetrodotoxin or delayed MK-801 , 1992, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[17]  J. Penney,et al.  Regional distribution and properties of [3H]MK-801 binding sites determined by quantitative autoradiography in rat brain , 1991, Neuroscience.

[18]  M. Reivich,et al.  Mechanism Underlying Protective Effect of MK-801 against NMDA-Induced Neuronal Injury in vivo , 1991, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[19]  J. Penney,et al.  Quisqualate‐ and NMDA‐sensitive [3H]glutamate binding in primate brain , 1990, Journal of neuroscience research.

[20]  M. Lauritzen,et al.  Influence of MK-801 on Brain Extracellular Calcium and Potassium Activities in Severe Hypoglycemia , 1990, Journal of Cerebral Blood Flow and Metabolism.

[21]  J. Mcculloch,et al.  Effects of NMDA antagonists, MK-801 and CPP, upon local cerebral glucose use , 1989, Brain Research.

[22]  R. Berne,et al.  Cerebral blood flow and interstitial fluid adenosine during hemorrhagic hypotension. , 1988, The American journal of physiology.

[23]  R. Auer Progress review: hypoglycemic brain damage. , 1986, Stroke.

[24]  T. Wieloch Hypoglycemia-induced neuronal damage prevented by an N-methyl-D-aspartate antagonist. , 1985, Science.

[25]  T. Wieloch,et al.  Lesions of the glutamatergic cortico-striatal projections in the rat ameliorate hypoglycemic brain damage in the striatum , 1985, Neuroscience Letters.

[26]  J I Hoffman,et al.  Blood flow measurements with radionuclide-labeled particles. , 1977, Progress in cardiovascular diseases.

[27]  K. Norberg,et al.  OXIDATIVE METABOLISM OF THE CEREBRAL CORTEX OF THE RAT IN SEVERE INSULIN‐INDUCED HYPOGLYCAEMIA , 1976, Journal of neurochemistry.

[28]  M. Koivisto,et al.  Neonatal Symptomatic and Asymptomatic Hypoglycaemia: A Follow‐up Study of 151 Children , 1972, Developmental medicine and child neurology.

[29]  J. Mccormack,et al.  Mitochondrial Ca2+ transport and the role of intramitochondrial Ca2+ in the regulation of energy metabolism. , 1993, Developmental neuroscience.

[30]  L. Sokoloff Sites and mechanisms of function-related changes in energy metabolism in the nervous system. , 1993, Developmental neuroscience.

[31]  U. Ungerstedt,et al.  The NMDA-antagonist MK-801 reduces extracellular amino acid levels during hypoglycemia and prevents striatal damage , 1988 .