Synaptic plasticity in the ischaemic brain
暂无分享,去创建一个
Antonio Pisani | Paolo Calabresi | P. Calabresi | D. Centonze | G. Bernardi | A. Pisani | L. Cupini | Giorgio Bernardi | Diego Centonze | Letizia M Cupini
[1] P. Gluckman,et al. Activity and injury-dependent expression of inducible transcription factors, growth factors and apoptosis-related genes within the central nervous system , 1999, Progress in Neurobiology.
[2] S. Hyman,et al. Addiction, Dopamine, and the Molecular Mechanisms of Memory , 2000, Neuron.
[3] Z. Xu,et al. Depression of Fast Excitatory Synaptic Transmission in Large Aspiny Neurons of the Neostriatum after Transient Forebrain Ischemia , 2002, The Journal of Neuroscience.
[4] W D Heiss,et al. Ischemic Penumbra: Evidence From Functional Imaging in Man , 2000, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[5] C. Hammond,et al. A selective LTP of NMDA receptor-mediated currents induced by anoxia in CA1 hippocampal neurons. , 1993, Journal of neurophysiology.
[6] Alain Buisson,et al. The proteolytic activity of tissue-plasminogen activator enhances NMDA receptor-mediated signaling , 2001, Nature Medicine.
[7] K. Hsu,et al. Characterization of the anoxia‐induced long‐term synaptic potentiation in area CA1 of the rat hippocampus , 1997, British journal of pharmacology.
[8] S. Warach. New imaging strategies for patient selection for thrombolytic and neuroprotective therapies , 2001, Neurology.
[9] Mark Hallett,et al. Plasticity of the human motor cortex and recovery from stroke , 2001, Brain Research Reviews.
[10] R. Nicoll,et al. Long-term potentiation--a decade of progress? , 1999, Science.
[11] N. Kawai,et al. Preconditioning In Vivo Ischemia Inhibits Anoxic Long-Term Potentiation and Functionally Protects CA1 Neurons in the Gerbil , 1998, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[12] B. Johansson,et al. Neuronal Plasticity and Dendritic Spines: Effect of Environmental Enrichment on Intact and Postischemic Rat Brain , 2002, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[13] T. Neumann-Haefelin,et al. Electrophysiological transcortical diaschisis after middle cerebral artery occlusion (MCAO) in rats , 1999, Neuroscience Letters.
[14] F. Plum. Neuroprotection in acute ischemic stroke. , 2001, JAMA.
[15] M E Greenberg,et al. Calcium signaling in neurons: molecular mechanisms and cellular consequences. , 1995, Science.
[16] T. Gao,et al. In vivo intracellular demonstration of an ischemia-induced postsynaptic potential from CA1 pyramidal neurons in rat hippocampus , 1996, Neuroscience.
[17] A. Buchan,et al. Continuing postischemic neuronal death in CA1: influence of ischemia duration and cytoprotective doses of NBQX and SNX-111 in rats. , 1999, Stroke.
[18] G. Dryhurst. Are dopamine, norepinephrine, and serotonin precursors of biologically reactive intermediates involved in the pathogenesis of neurodegenerative brain disorders? , 2001, Advances in experimental medicine and biology.
[19] G. Hagemann,et al. Electrophysiological transcortical diaschisis after cortical photothrombosis in rat brain. , 1996, Stroke.
[20] K. Krnjević,et al. 2-Deoxyglucose-induced long-term potentiation in CA1 is not prevented by intraneuronal chelator. , 2000, Journal of neurophysiology.
[21] E. Kumral,et al. Acute caudate vascular lesions. , 1999, Stroke.
[22] P. Calabresi,et al. Ionic mechanisms underlying differential vulnerability to ischemia in striatal neurons , 2001, Progress in Neurobiology.
[23] Cornelius Weiller,et al. Recovery of motor and language abilities after stroke: the contribution of functional imaging , 2002, Progress in neurobiology.
[24] T. Neumann-Haefelin,et al. Increased long‐term potentiation in the surround of experimentally induced focal cortical infarction , 1998, Annals of neurology.
[25] P. Rossini,et al. Post-stroke plastic reorganisation in the adult brain , 2003, The Lancet Neurology.
[26] P. Calabresi,et al. Tissue plasminogen activator is required for striatal post-ischemic synaptic potentiation , 2002, Neuroreport.
[27] R. Sapolsky,et al. Neuronal apoptosis in acute necrotic insults: why is this subject such a mess? , 1999, Trends in Neurosciences.
[28] C. Hammond,et al. Anoxia-induced LTP of isolated NMDA receptor-mediated synaptic responses. , 1993, Journal of neurophysiology.
[29] P. Calabresi,et al. Striatal spiny neurons and cholinergic interneurons express differential ionotropic glutamatergic responses and vulnerability: Implications for ischemia and Huntington's disease , 1998, Annals of neurology.
[30] J. Lodder,et al. Stroke and idiopathic Parkinson's disease: Does a shortage of dopamine offer protection against stroke? , 2001, Movement disorders : official journal of the Movement Disorder Society.
[31] Y. Ben‐Ari,et al. Anoxic LTP is mediated by the redox modulatory site of the NMDA receptor. , 1994, Journal of neurophysiology.
[32] Mark Ellisman,et al. Alterations of hippocampal postsynaptic densities following transient ischemia , 2000, Hippocampus.
[33] K. Krnjević,et al. Calcium dependence of LTP induced by 2-deoxyglucose in CA1 neurons. , 1996, Journal of neurophysiology.
[34] K. Hossmann. Viability thresholds and the penumbra of focal ischemia , 1994, Annals of neurology.
[35] Yildirim Sara,et al. Persistent Defect in Transmitter Release and Synapsin Phosphorylation in Cerebral Cortex After Transient Moderate Ischemic Injury , 2002, Stroke.
[36] G Bernardi,et al. Activation of metabotropic glutamate receptor subtype 1/protein kinase C/mitogen-activated protein kinase pathway is required for postischemic long-term potentiation in the striatum. , 2001, Molecular pharmacology.
[37] M. Mattson,et al. Caspase and calpain substrates: Roles in synaptic plasticity and cell death , 1999, Journal of neuroscience research.
[38] P. Calabresi,et al. Is pharmacological neuroprotection dependent on reduced glutamate release? , 2000, Stroke.
[39] T. Gao,et al. Prolonged enhancement and depression of synaptic transmission in CA1 pyramidal neurons induced by transient forebrain ischemia in vivo , 1998, Neuroscience.
[40] H. Bokura,et al. Long-term cognitive impairment associated with caudate stroke. , 1997, Stroke.
[41] K. Hsu,et al. Nitric Oxide Signalling is Required for the Generation of Anoxia‐induced Long‐term Potentiation in the Hippocampus , 1997, The European journal of neuroscience.
[42] M. Mattson,et al. Dietary restriction normalizes glucose metabolism and BDNF levels, slows disease progression, and increases survival in huntingtin mutant mice , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[43] D. H. Mellor,et al. Real time , 1981 .
[44] Y. Goshima,et al. Endogenously released DOPA is a causal factor for glutamate release and resultant delayed neuronal cell death by transient ischemia in rat striata , 2001, Journal of neurochemistry.
[45] Y. Ben‐Ari,et al. Intracellular injection of a Ca2+ chelator prevents generation of anoxic LTP. , 1996, Journal of neurophysiology.
[46] C. Hammond,et al. Anoxic LTP sheds light on the multiple facets of NMDA receptors , 1994, Trends in Neurosciences.
[47] R. Malinow,et al. Transient oxygen–glucose deprivation induces rapid morphological changes in rat hippocampal dendrites , 2001, Neuropharmacology.
[48] P. Calabresi,et al. Post-ischaemic long-term synaptic potentiation in the striatum: a putative mechanism for cell type-specific vulnerability. , 2002, Brain : a journal of neurology.
[49] J. Wardlaw,et al. Systematic Review of Diffusion and Perfusion Imaging in Acute Ischemic Stroke , 2000, Stroke.
[50] F. Barone,et al. Pharmacological interventions for stroke: failures and future , 2002, Expert opinion on investigational drugs.
[51] A. Buisson,et al. Striatal Protection Induced by Lesioning the Substantia Nigra of Rats Subjected to Focal Ischemia , 1992, Journal of neurochemistry.
[52] J. Stamford,et al. ‘Real time’ measurement of dopamine release in an in vitro model of neostriatal ischaemia , 1996, Journal of Neuroscience Methods.
[53] J. Sandkühler,et al. Inhibition of caspases prevents cell death of hippocampal CA1 neurons, but not impairment of hippocampal long-term potentiation following global ischemia , 1999, Neuroscience.
[54] Y. Ben-Ari. Cell Death and Synaptic Reorganizations Produced by Seizures , 2001, Epilepsia.
[55] M. Mattson. Apoptotic and Anti‐Apoptotic Synaptic Signaling Mechanisms , 2000, Brain pathology.
[56] Mark H. Ellisman,et al. Modification of Postsynaptic Densities after Transient Cerebral Ischemia: A Quantitative and Three-Dimensional Ultrastructural Study , 1999, The Journal of Neuroscience.
[57] W. Low,et al. Alterations in striatal dopamine release and reuptake under conditions of mild, moderate, and severe cerebral ischemia. , 1995, Neurosurgery.
[58] Mark P Mattson,et al. Calcium signaling in the ER: its role in neuronal plasticity and neurodegenerative disorders , 2000, Trends in Neurosciences.
[59] R. Yuste,et al. Morphological changes in dendritic spines associated with long-term synaptic plasticity. , 2001, Annual review of neuroscience.
[60] R. L. Büyükuysal,et al. Anoxia‐Induced Dopamine Release from Rat Striatal Slices , 1999, Journal of neurochemistry.
[61] Jeff Biernaskie,et al. Enriched Rehabilitative Training Promotes Improved Forelimb Motor Function and Enhanced Dendritic Growth after Focal Ischemic Injury , 2001, The Journal of Neuroscience.
[62] M. Moskowitz,et al. Pathobiology of ischaemic stroke: an integrated view , 1999, Trends in Neurosciences.
[63] Joseph P. Broderick,et al. Tissue plasminogen activator for acute ischemic stroke. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. , 1995 .
[64] M. Mattson,et al. Meal size and frequency affect neuronal plasticity and vulnerability to disease: cellular and molecular mechanisms , 2003, Journal of neurochemistry.
[65] P. Calabresi,et al. Sodium influx plays a major role in the membrane depolarization induced by oxygen and glucose deprivation in rat striatal spiny neurons. , 1999, Stroke.
[66] Protein kinase C inhibitors block generation of anoxia‐induced long‐term potentiation , 1998, Neuroreport.
[67] F. Müller,et al. Effect of levodopa in combination with physiotherapy on functional motor recovery after stroke: a prospective, randomised, double-blind study , 2001, The Lancet.
[68] Christopher A. Shaw,et al. An alternative to the LTP orthodoxy: a plasticity-pathology continuum model , 1996, Brain Research Reviews.
[69] Jeffry R Alger,et al. Late secondary ischemic injury in patients receiving intraarterial thrombolysis , 2002, Annals of neurology.
[70] D. Muller,et al. Remodeling of Hippocampal Synaptic Networks by a Brief Anoxia–Hypoglycemia , 2002, The Journal of Neuroscience.
[71] S. J. Martin,et al. Synaptic plasticity and memory: an evaluation of the hypothesis. , 2000, Annual review of neuroscience.
[72] Z. C. Xu,et al. Differential changes of synaptic transmission in spiny neurons of rat neostriatum following transient forebrain ischemia , 2001, Neuroscience.
[73] W. Pulsinelli. Selective neuronal vulnerability: morphological and molecular characteristics. , 1985, Progress in brain research.
[74] K. Zilles,et al. Widespread up-regulation of N-methyl-d-aspartate receptors after focal photothrombotic lesion in rat brain , 1999, Neuroscience Letters.
[75] M. Mattson,et al. Evidence that brain‐derived neurotrophic factor is required for basal neurogenesis and mediates, in part, the enhancement of neurogenesis by dietary restriction in the hippocampus of adult mice , 2002, Journal of neurochemistry.
[76] Yitao Liu,et al. Treatment of Ischemic Brain Damage by Perturbing NMDA Receptor- PSD-95 Protein Interactions , 2002, Science.
[77] P. Calabresi,et al. Endogenous Dopamine Amplifies Ischemic Long-Term Potentiation via D1 Receptors , 2002, Stroke.
[78] Jin-Moo Lee,et al. The changing landscape of ischaemic brain injury mechanisms , 1999, Nature.
[79] H. Bolay,et al. Mechanisms of motor dysfunction after transient MCA occlusion: persistent transmission failure in cortical synapses is a major determinant. , 1998, Stroke.
[80] H. Gozlan,et al. NMDA receptor redox sites: are they targets for selective neuronal protection? , 1995, Trends in pharmacological sciences.
[81] P. Calabresi,et al. Cellular factors controlling neuronal vulnerability in the brain , 2000, Neurology.
[82] P. Calabresi,et al. The corticostriatal projection: from synaptic plasticity to dysfunctions of the basal ganglia , 1996, Trends in Neurosciences.