NR2B-containing NMDA receptors promote the neurotoxic effects of 3-nitropropionic acid but not of rotenone in the striatum.

No abstract is available for this paper.

• Publication year

  2006

• Venue

  Experimental Neurology

• Publication date

  2006-12-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1016/J.EXPNEUROL.2006.07.009PMID 16919272
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Huntington's disease

  2007cited by this paper
• Disturbed Ca2+ signaling and apoptosis of medium spiny neurons in Huntington's disease.

  2005cited by this paper
• Partial Mitochondrial Inhibition Causes Striatal Dopamine Release Suppression and Medium Spiny Neuron Depolarization via H2O2 Elevation, Not ATP Depletion

  2005cited by this paper
• NR2A and NR2B receptor gene variations modify age at onset in Huntington disease

  2005cited by this paper
• Quantification of acetogenins in Annona muricata linked to atypical parkinsonism in guadeloupe

  2005cited by this paper
• The mitochondrial complex I inhibitor rotenone triggers a cerebral tauopathy

  2005cited by this paper
• Early ionic and membrane potential changes caused by the pesticide rotenone in striatal cholinergic interneurons.

  2004cited by this paper
• Effects of mitochondrial dysfunction on glutamate receptor-mediated neurotoxicity in cultured rat spinal motor neurons.

  2004cited by this paper
• Variable effects of chronic subcutaneous administration of rotenone on striatal histology

  2004cited by this paper
• Neuronal vulnerability following inhibition of mitochondrial complex II: a possible ionic mechanism for Huntington's disease.

  2004cited by this paper
• Coactivation of GABAA and GABAB Receptor Results in Neuroprotection During In Vitro Ischemia

  2004cited by this paper
• Inhibition of mitochondrial complex II alters striatal expression of genes involved in glutamatergic and dopaminergic signaling: possible implications for Huntington's disease.

  2004cited by this paper
• Rotenone induces non‐specific central nervous system and systemic toxicity

  2004cited by this paper
• Transient and Progressive Electrophysiological Alterations in the Corticostriatal Pathway in a Mouse Model of Huntington's Disease

  2003cited by this paper
• The mitochondrial complex I inhibitor annonacin is toxic to mesencephalic dopaminergic neurons by impairment of energy metabolism.

  2003cited by this paper
• Chronic systemic complex I inhibition induces a hypokinetic multisystem degeneration in rats

  2003cited by this paper
• Annonacin, a lipophilic inhibitor of mitochondrial complex I, induces nigral and striatal neurodegeneration in rats: possible relevance for atypical parkinsonism in Guadeloupe

  2003cited by this paper
• The N-methyl-D-aspartate receptor subunit NR2B: localization, functional properties, regulation, and clinical implications.

  2003cited by this paper
• Role of NR2B-type NMDA receptors in selective neurodegeneration in Huntington disease.

  2003cited by this paper
• Ionotropic glutamate receptors: still a target for neuroprotection in brain ischemia? Insights from in vitro studies.

  2003cited by this paper
• Role of nitric oxide in rotenone‐induced nigro‐striatal injury

  2003cited by this paper
• Subcutaneous rotenone exposure causes highly selective dopaminergic degeneration and alpha-synuclein aggregation.

  2003cited by this paper
• Dopamine is involved in selectivity of dopaminergic neuronal death by rotenone

  2003cited by this paper
• Lamotrigine and remacemide protect striatal neurons against in vitro ischemia: an electrophysiological study.

  2003cited by this paper
• Ifenprodil and ethanol enhance NMDA receptor-dependent long-term depression.

  2002cited by this paper
• Extrasynaptic NMDARs oppose synaptic NMDARs by triggering CREB shut-off and cell death pathways

  2002cited by this paper
• Mitochondrial dysfunction in progressive supranuclear palsy.

  2002cited by this paper
• Excitotoxicity: perspectives based on N-methyl-D-aspartate receptor subtypes.

  2002cited by this paper
• Voxel-based comparison of regional cerebral glucose metabolism between PSP and corticobasal degeneration.

  2002cited by this paper
• Guadeloupean parkinsonism: a cluster of progressive supranuclear palsy-like tauopathy.

  2002cited by this paper
• Increased sensitivity to N-methyl-D-aspartate receptor-mediated excitotoxicity in a mouse model of Huntington's disease.

  2002cited by this paper
• Cholinergic vesicular transporters in progressive supranuclear palsy

  2002cited by this paper
• The mechanisms of neuronal death produced by mitochondrial toxin 3-nitropropionic acid: the roles of N-methyl-D-aspartate glutamate receptors and mitochondrial calcium overload.

  2002cited by this paper
• Stress-induced mitochondrial depolarization and oxidative damage in PSP cybrids.

  2002cited by this paper
• An abnormal striatal synaptic plasticity may account for the selective neuronal vulnerability in Huntington's disease

  2001cited by this paper
• Inhibition of Mitochondrial Complex II Induces a Long-Term Potentiation of NMDA-Mediated Synaptic Excitation in the Striatum Requiring Endogenous Dopamine

  2001cited by this paper
• Further evidence for mitochondrial dysfunction in progressive supranuclear palsy.

  2001cited by this paper
• Inhibition of glutamate uptake into synaptic vesicles from rat brain by 3-nitropropionic acid in vitro.

  2001cited by this paper
• NMDA receptor function in mouse models of Huntington disease

  2001cited by this paper
• Loss of Huntingtin-Mediated BDNF Gene Transcription in Huntington's Disease

  2001cited by this paper
• Mitochondrial Dysfunction in Cybrid Lines Expressing Mitochondrial Genes from Patients with Progressive Supranuclear Palsy

  2000cited by this paper
• Deficit of brain and skeletal muscle bioenergetics in progressive supranuclear palsy shown in vivo by phosphorus magnetic resonance spectroscopy

  2000cited by this paper
• Neuronal cell death in Huntington's disease: a potential role for dopamine.

  2000cited by this paper
• Delayed Mitochondrial Dysfunction in Excitotoxic Neuron Death: Cytochrome c Release and a Secondary Increase in Superoxide Production

  2000cited by this paper
• Chemical anatomy of striatal interneurons in normal individuals and in patients with Huntington's disease.

  2000cited by this paper
• Is pharmacological neuroprotection dependent on reduced glutamate release?

  2000cited by this paper
• Possible relation of atypical parkinsonism in the French West Indies with consumption of tropical plants: a case-control study. Caribbean Parkinsonism Study Group.

  1999cited by this paper
• Antagonists selective for NMDA receptors containing the NR2B subunit.

  1999cited by this paper
• Oxidative Stress, Mitochondrial Function, and Acute Glutamate Excitotoxicity in Cultured Cerebellar Granule Cells

  1999cited by this paper
• Differential vulnerability of dopamine receptors in the mouse brain treated with MPTP.

  1999cited by this paper
• Striatal dopamine depletion and behavioural sensitization induced by methamphetamine and 3-nitropropionic acid.

  1999cited by this paper
• Possible relation of atypical parkinsonism in the French West Indies with consumption of tropical plants: a case-control study

  1999cited by this paper
• 6-Hydroxydopamine injections into the nigrostriatal pathway attenuate striatal malonate and 3-nitropropionic acid lesions.

  1998cited by this paper
• Dopamine Modulates the Susceptibility of Striatal Neurons to 3-Nitropropionic Acid in the Rat Model of Huntington’s Disease

  1998cited by this paper
• Huntington disease.

  1998cited by this paper
• Systemic administration of rotenone produces selective damage in the striatum and globus pallidus, but not in the substantia nigra.

  1997cited by this paper
• Oxidative damage and metabolic dysfunction in Huntington's disease: Selective vulnerability of the basal ganglia

  1997cited by this paper
• Mitochondrial toxin 3-nitropropionic acid produces startle reflex abnormalities and striatal damage in rats that model some features of Huntington's disease.

  1997cited by this paper
• Chronic 3-Nitropropionic Acid Treatment in Baboons Replicates the Cognitive and Motor Deficits of Huntington’s Disease

  1996cited by this paper
• Mitochondrial defect in Huntington's disease caudate nucleus

  1996cited by this paper
• Bioenergetics and glutamate excitotoxicity.

  1996cited by this paper
• The clinical and pathological spectrum of Steele-Richardson-Olszewski syndrome (progressive supranuclear palsy): a reappraisal.

  1995cited by this paper
• Chronic mitochondrial energy impairment produces selective striatal degeneration and abnormal choreiform movements in primates.

  1995cited by this paper
• Neurochemistry and toxin models in Huntington's disease.

  1994cited by this paper
• 3‐Nitropropionic Acid Toxicity in the Striatum

  1994cited by this paper
• Preliminary NINDS neuropathologic criteria for Steele‐Richardson‐Olszewski syndrome (progressive supranuclear palsy)

  1994cited by this paper
• A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes. The Huntington's Disease Collaborative Research Group.

  1993cited by this paper
• A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes. The Huntington's Disease Collaborative Research Group.

  1993cited by this paper
• 3-Nitropropionic Acid - Exogenous Animal Neurotoxin and Possible Human Striatal Toxin

  1991cited by this paper
• Large neurons in the neostriatum in Alzheimer's disease and progressive supranuclear palsy: a topographic, histologic and ultrastructural investigation.

  1991cited by this paper
• Cerebral hypometabolism in progressive supranuclear palsy studied with positron emission tomography

  1988cited by this paper
• Dopaminergic and cholinergic lesions in progressive supranuclear palsy

  1985cited by this paper
• Selective sparing of a class of striatal neurons in Huntington's disease.

  1985cited by this paper
• Journal of Cerebral Blood Flow and Metabolism Excitotoxicity Is Required for Induction of Oxidative Stress and Apoptosis in Mouse Striatum by the Mitochondrial Toxin, 3-nitropropionic Acid

  year unknowncited by this paper

• An Update of Kaempferol Protection against Brain Damage Induced by Ischemia-Reperfusion and by 3-Nitropropionic Acid

  2024cites this paper
• The three sisters of fate: Genetics, pathophysiology and outcomes of animal models of neurodegenerative diseases.

  2022cites this paper
• Exaggerated mitophagy: a weapon of striatal destruction in the brain?

  2020cites this paper
• Neutrophil-selective deletion of Cxcr2 protects against CNS neurodegeneration in a mouse model of multiple sclerosis

  2020cites this paper
• Neuronal adenosine A2A receptor overexpression is neuroprotective towards 3-nitropropionic acid-induced striatal toxicity: a rat model of Huntington’s disease

  2018cites this paper
• Neurotoxic Agent-Induced Injury in Neurodegenerative Disease Model: Focus on Involvement of Glutamate Receptors

  2018cites this paper
• Microglial activation and the nitric oxide/cGMP/PKG pathway underlie enhanced neuronal vulnerability to mitochondrial dysfunction in experimental multiple sclerosis.

  2018cites this paper
• Nrf2 pathway activation upon rotenone treatment in human iPSC‐derived neural stem cells undergoing differentiation towards neurons and astrocytes

  2017cites this paper
• Neuronal oscillations: A physiological correlate for targeting mitochondrial dysfunction in neurodegenerative diseases?

  2016cites this paper
• Alpha-synuclein modulates NR2B-containing NMDA receptors and decreases their levels after rotenone exposure.

  2015cites this paper
• Interleukin-1β causes excitotoxic neurodegeneration and multiple sclerosis disease progression by activating the apoptotic protein p53

  2014cites this paper
• Interferon-β1a protects neurons against mitochondrial toxicity via modulation of STAT1 signaling: electrophysiological evidence.

  2014cites this paper
• Brief mitochondrial inhibition causes lasting changes in motor behavior and corticostriatal synaptic physiology in the Fischer 344 rat.

  2012cites this paper
• Interleukin‐1β causes synaptic hyperexcitability in multiple sclerosis

  2012cites this paper
• The NMDA receptor subunit GluN3A protects against 3-nitroproprionic-induced striatal lesions via inhibition of calpain activation.

  2012cites this paper
• Estudi de la neurodegeneració i les alteracions de la barrera hematoencefàlica en rates tractades amb àcid 3-nitropropiònic

  2012cites this paper
• NR2B subunit blockade does not affect motor symptoms induced by 3-nitropropionic acid

  2011cites this paper
• Mortalin inhibition in experimental Parkinson's disease

  2011cites this paper
• Downstream mechanisms triggered by mitochondrial dysfunction in the basal ganglia: from experimental models to neurodegenerative diseases.

  2010cites this paper
• Electrophysiological actions of zonisamide on striatal neurons: Selective neuroprotection against complex I mitochondrial dysfunction.

  2010cites this paper
• Induction of heat shock protein 70 reduces the alteration of striatal electrical activity caused by mitochondrial impairment.

  2009cites this paper
• A2A adenosine receptor antagonists protect the striatum against rotenone-induced neurotoxicity.

  2009cites this paper
• Blood-brain barrier disruption in the striatum of rats treated with 3-nitropropionic acid.

  2009cites this paper
• Kaempferol protects against rat striatal degeneration induced by 3‐nitropropionic acid

  2009cites this paper
• Cortical and brainstem LTP-like plasticity in Huntington's disease.

  2008cites this paper
• Electrophysiology and Pharmacology of Striatal Neuronal Dysfunction Induced by Mitochondrial Complex I Inhibition

  2008cites this paper
• Memantine reduces neuronal dysfunctions triggered by in vitro ischemia and 3-nitropropionic acid.

  2007cites this paper