1-Methyl-1,2,3,4-tetrahydroisoquinoline and established uncompetitive NMDA receptor antagonists induce tolerance to excitotoxicity

[1]  W. Gordon-Krajcer,et al.  Homocysteine-induced acute excitotoxicity in cerebellar granule cells in vitro is accompanied by PP2A-mediated dephosphorylation of tau , 2009, Neurochemistry International.

[2]  J. Michaluk,et al.  1-Methyl-1,2,3,4-tetrahydroisoquinoline Antagonizes a Rise in Brain Dopamine Metabolism, Glutamate Release in Frontal Cortex and Locomotor Hyperactivity Produced by MK-801 but not the Disruptions of Prepulse Inhibition, and Impairment of Working Memory in Rat , 2009, Neurotoxicity Research.

[3]  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.

[4]  U. Dirnagl,et al.  Preconditioning and tolerance against cerebral ischaemia: from experimental strategies to clinical use , 2009, The Lancet Neurology.

[5]  J. Burda,et al.  Effect of Antioxidant Treatment in Global Ischemia and Ischemic Postconditioning in the Rat Hippocampus , 2009, Cellular and Molecular Neurobiology.

[6]  J. Burda,et al.  Postconditioning and Anticonditioning: Possibilities to Interfere to Evoked Apoptosis , 2009, Cellular and Molecular Neurobiology.

[7]  E. Neafsey,et al.  Alcohol in moderation, cardioprotection, and neuroprotection: epidemiological considerations and mechanistic studies. , 2009, Alcoholism, clinical and experimental research.

[8]  Z. Xiong,et al.  Differential Roles of NMDA Receptor Subtypes in Ischemic Neuronal Cell Death and Ischemic Tolerance , 2008, Stroke.

[9]  F. Moroni,et al.  Neuroprotection by group I mGlu receptors in a rat hippocampal slice model of cerebral ischemia is associated with the PI3K–Akt signaling pathway: A novel postconditioning strategy? , 2008, Neuropharmacology.

[10]  Min Zhang,et al.  Ischemic Postconditioning Inhibits Apoptosis After Focal Cerebral Ischemia/Reperfusion Injury in the Rat , 2008, Stroke.

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

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

[13]  R. Simon,et al.  In Vivo and In Vitro Characterization of a Novel Neuroprotective Strategy for Stroke: Ischemic Postconditioning , 2008 .

[14]  Nicholas P. Franks,et al.  Competitive Inhibition at the Glycine Site of the N-Methyl-d-aspartate Receptor by the Anesthetics Xenon and Isoflurane: Evidence from Molecular Modeling and Electrophysiology , 2007, Anesthesiology.

[15]  Á. Simonyi,et al.  Ethanol preconditioning protects against ischemia/reperfusion‐induced brain damage: Role of NADPH oxidase‐derived ROS , 2007, Free radical biology & medicine.

[16]  Nirmal Singh,et al.  Role of phosphoinositide 3-kinase in ischemic postconditioning-induced attenuation of cerebral ischemia-evoked behavioral deficits in mice. , 2007, Pharmacological reports : PR.

[17]  K. Wanner,et al.  Affinity of 1-aryl-1,2,3,4-tetrahydroisoquinoline derivatives to the ion channel binding site of the NMDA receptor complex. , 2006, European journal of medicinal chemistry.

[18]  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.

[19]  M. Kajta,et al.  The mechanism of 1,2,3,4‐tetrahydroisoquinolines neuroprotection: the importance of free radicals scavenging properties and inhibition of glutamate‐induced excitotoxicity , 2006, Journal of neurochemistry.

[20]  J. Burda,et al.  Delayed Postconditionig Initiates Additive Mechanism Necessary for Survival of Selectively Vulnerable Neurons After Transient Ischemia in Rat Brain , 2006, Cellular and Molecular Neurobiology.

[21]  Toshiaki Saitoh,et al.  Synthesis and neurotoxicity of tetrahydroisoquinoline derivatives for studying Parkinson's disease. , 2005, Biological & pharmaceutical bulletin.

[22]  D. Pei,et al.  Neuroprotective Effects of Preconditioning Ischemia on Ischemic Brain Injury through Down-regulating Activation of JNK1/2 via N-Methyl-D-aspartate Receptor-mediated Akt1 Activation* , 2005, Journal of Biological Chemistry.

[23]  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.

[24]  S. Lipton The molecular basis of memantine action in Alzheimer's disease and other neurologic disorders: low-affinity, uncompetitive antagonism. , 2005, Current Alzheimer research.

[25]  Claudia M Testa,et al.  Rotenone induces oxidative stress and dopaminergic neuron damage in organotypic substantia nigra cultures. , 2005, Brain research. Molecular brain research.

[26]  Katsuhiro Okuda,et al.  Neuroprotective effect of 1-methyl-1,2,3,4-tetrahydroisoquinoline on cultured rat mesencephalic neurons in the presence or absence of various neurotoxins , 2005, Brain Research.

[27]  R. Bordet,et al.  Brain ischemic preconditioning is abolished by antioxidant drugs but does not up-regulate superoxide dismutase and glutathion peroxidase , 2004, Brain Research.

[28]  L. Antkiewicz‐Michaluk,et al.  Inhibition of rodent brain monoamine oxidase and tyrosine hydroxylase by endogenous compounds - 1,2,3,4-tetrahydro-isoquinoline alkaloids. , 2004, Polish journal of pharmacology.

[29]  A. Bojarski,et al.  Protective effect of 1-methyl-1,2,3,4-tetrahydroisoquinoline against dopaminergic neurodegeneration in the extrapyramidal structures produced by intracerebral injection of rotenone. , 2004, The international journal of neuropsychopharmacology.

[30]  N. Diemer,et al.  MK-801 does not prevent development of ischemic tolerance in rat brain , 2004, Neuroreport.

[31]  M. Tymianski,et al.  Molecular mechanisms of calcium-dependent neurodegeneration in excitotoxicity. , 2003, Cell calcium.

[32]  A. Bojarski,et al.  1-methyl-1,2,3,4-tetrahydroisoquinoline protects against rotenone-induced mortality and biochemical changes in rat brain. , 2003, European journal of pharmacology.

[33]  S. Ohta,et al.  Different action on dopamine catabolic pathways of two endogenous 1,2,3,4‐tetrahydroisoquinolines with similar antidopaminergic properties , 2001, Journal of neurochemistry.

[34]  R. Tremblay,et al.  Transient NMDA Receptor Inactivation Provides Long-Term Protection to Cultured Cortical Neurons from a Variety of Death Signals , 2000, The Journal of Neuroscience.

[35]  A. Szczudlik,et al.  Neurochemical changes induced by acute and chronic administration of 1,2,3,4-tetrahydroisoquinoline and salsolinol in dopaminergic structures of rat brain , 2000, Neuroscience.

[36]  Yuji Ueda,et al.  Intracellular Survival Pathways against Glutamate Receptor Agonist Excitotoxicity in Cultured Neurons: Intracellular Calcium Responsesa , 1999, Annals of the New York Academy of Sciences.

[37]  S. Wolfarth,et al.  Effect of acute and chronic administration of 1,2,3,4-tetrahydroisoquinoline on muscle tone, metabolism of dopamine in the striatum and tyrosine hydroxylase immunocytochemistry in the substantia nigra, in rats , 1999, Neuroscience.

[38]  M. O'Neill,et al.  NMDA receptor antagonism, but not AMPA receptor antagonism attenuates induced ischaemic tolerance in the gerbil hippocampus. , 1999, European journal of pharmacology.

[39]  J. Koh,et al.  N-Methyl- d -aspartate Receptor Blockade Induces Neuronal Apoptosis in Cortical Culture , 1999, Experimental Neurology.

[40]  A. Schousboe Pharmacologic and therapeutic aspects of the developmentally regulated expression of GABAA and GABAB receptors: cerebellar granule cells as a model system , 1999, Neurochemistry International.

[41]  Y. Minabe,et al.  Rolipram, a Selective Phosphodiesterase Type‐IV Inhibitor, Prevents Induction of Heat Shock Protein HSP‐70 and hsp‐70 mRNA in Rat Retrosplenial Cortex by the NMDA Receptor Antagonist DizociIpine , 1997, The European journal of neuroscience.

[42]  C. J. Schmidt,et al.  Regional effects of MK-801 on dopamine release: effects of competitive NMDA or 5-HT2A receptor blockade. , 1996, The Journal of pharmacology and experimental therapeutics.

[43]  S. Ohta,et al.  1‐Benzyl‐1,2,3,4‐Tetrahydroisoquinoline as a Parkinsonism‐Inducing Agent: A Novel Endogenous Amine in Mouse Brain and Parkinsonian CSF , 1995, Journal of neurochemistry.

[44]  S. Lipton,et al.  Glutamate-induced neuronal death: A succession of necrosis or apoptosis depending on mitochondrial function , 1995, Neuron.

[45]  J. Prehn,et al.  Are NMDA or AMPA/kainate receptor antagonists more efficacious in the delayed treatment of excitotoxic neuronal injury? , 1995, European journal of pharmacology.

[46]  N. Tashiro,et al.  Effect of phenycyclidine on dopamine release in the rat prefrontal cortex; an in vivo microdialysis study , 1994, Brain Research.

[47]  Yong Liu,et al.  MK-801, but not anisomycin, inhibits the induction of tolerance to ischemia in the gerbil hippocampus , 1992, Neuroscience Letters.

[48]  S. Ohta,et al.  1‐Methyl‐ 1,2,3,4‐Tetrahydroisoquinoline, Decreasing in 1‐Methyl‐4‐Phenyl‐1,2,3,6‐Tetrahydropyridine‐Treated Mouse, Prevents Parkinsonism‐Like Behavior Abnormalities , 1991, Journal of neurochemistry.

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

[50]  P. Contreras,et al.  Phencyclidine-like effects of tetrahydroisoquinolines and related compounds. , 1989, Journal of medicinal chemistry.

[51]  G White,et al.  Ethanol inhibits NMDA-activated ion current in hippocampal neurons. , 1989, Science.

[52]  R. Gill,et al.  Neuroprotective effects of MK-801 in vivo: selectivity and evidence for delayed degeneration mediated by NMDA receptor activation , 1988, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[53]  S. Rothman,et al.  Delayed neurotoxicity of excitatory amino acids In vitro , 1987, Neuroscience.

[54]  S. Lipton Failures and successes of NMDA receptor antagonists: Molecular basis for the use of open-channel blockers like memantine in the treatment of acute and chronic neurologic insults , 2011, NeuroRX.

[55]  R Rossaint,et al.  Xenon: recent developments and future perspectives. , 2009, Minerva anestesiologica.

[56]  J. Vetulani,et al.  A possible physiological role for cerebral tetrahydroisoquinolines , 2009, Neurotoxicity Research.

[57]  W. Danysz,et al.  NMDA receptor antagonism does not inhibit induction of ischemic tolerance in gerbil brainin vivo , 2009, Neurotoxicity Research.

[58]  A. Contestabile Cerebellar granule cells as a model to study mechanisms of neuronal apoptosis or survivalin vivo andin vitro , 2008, The Cerebellum.

[59]  T. Obrenovitch Molecular physiology of preconditioning-induced brain tolerance to ischemia. , 2008, Physiological reviews.

[60]  S. Lipton,et al.  Emerging roles of S-nitrosylation in protein misfolding and neurodegenerative diseases. , 2008, Antioxidants & redox signaling.

[61]  D. Ray,et al.  Antioxidants attenuate MK-801-induced cortical neurotoxicity in the rat. , 2007, Neurotoxicology.

[62]  N. Tashiro,et al.  Effect of phencyclidine on dopamine release in the rat prefrontal cortex; an in vivo microdialysis study. , 1994, Brain research.

[63]  A. Schousboe,et al.  Cultured neurons as model systems for biochemical and pharmacological studies on receptors for neurotransmitter amino acids. , 1985, Developmental neuroscience.