1-Methyl-1,2,3,4-tetrahydroisoquinoline and established uncompetitive NMDA receptor antagonists induce tolerance to excitotoxicity
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E. Salińska | L. Antkiewicz-Michaluk | M. Slomka | M. Kuszczyk | J. Łazarewicz | L. Antkiewicz‐Michaluk
[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.