Dearth of glutamate transporters contributes to striatal excitotoxicity.
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Summary
The relative expression levels of glutamate transporters, even in parts of the brain where they are considered adequately expressed, appear to influence the sensitivities of different neuronal populations to excitotoxicity.
- Type
- article
- Published
- 2004-10-01
- Cited by
- 34
- References
- 66
- OpenAlex
- https://openalex.org/W2048616485
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:36929918
Keywords
Excitotoxicity, Glutamate receptor, NMDA receptor, Hippocampal formation, Biology
References
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- Non-NMDA receptor-mediated neurotoxicity in cortical culture
- Neuronal Glutamate Uptake Contributes to GABA Synthesis and Inhibitory Synaptic Strength
- Development of inhibitory synapses among striatal neurons in vitro
- Differential expression of two glial glutamate transporters in the rat brain: quantitative and immunocytochemical observations
- Intracellular calcium concentrations during "chemical hypoxia" and excitotoxic neuronal injury
- Impaired glutamate uptake in the R6 Huntington's disease transgenic mice.
- Dihydrokainate‐sensitive neuronal glutamate transport is required for protection of rat cortical neurons in culture against synaptically released glutamate
- Inhibition of uptake unmasks rapid extracellular turnover of glutamate of nonvesicular origin.
- Differential synaptic localization of the glutamate transporter EAAC1 and glutamate receptor subunit gluR2 in the rat hippocampus
- Age‐Dependent Vulnerability of the Striatum to the Mitochondrial Toxin 3‐Nitropropionic Acid
- Mutant huntingtin enhances excitotoxic cell death.
- Cultured astrocytes express regional heterogeneity of the immunoreactive phenotype under basal conditions and after gamma-IFN induction.
Cited by
- Downregulation of spinal glutamate transporter EAAC1 followingnerve injury is regulated by central glucocorticoid receptors in rats
- Presymptomatic Glutamate Levels in Prefrontal Cortex in the Hdh(CAG150) Mouse Model of Huntington's Disease
- The role of the nmda receptor and reverse sodium calcium exchanger in calcium dysregulation in glutamate-exposed neurons
- Huntingtin Nuclear Localization: Current Insights into Mechanism and Regulation
- Genetic analysis of the GRIK2 modifier effect in Huntington's disease
- Anti-superoxide and anti-peroxynitrite strategies in pain suppression
- Calpain Activation and Na/Ca Exchanger Degradation Occur Downstream of Calcium Deregulation in Hippocampal Neurons Exposed to Excitotoxic Glutamate
- Glutamate-glutamine cycling in Alzheimer's disease.
- Detergent-Insoluble EAAC1/EAAT3 Aberrantly Accumulates in Hippocampal Neurons of Alzheimer’s Disease Patients
- Delayed calcium dysregulation in neurons requires both the NMDA receptor and the reverse Na+/Ca2+ exchanger
- Decreased expression of GLT-1 in the R6/2 model of Huntington’s disease does not worsen disease progression
- Peroxynitrite and Opiate Antinociceptive Tolerance: A Painful Reality
- HACE1 reduces oxidative stress and mutant Huntingtin toxicity by promoting the NRF2 response
- The role of glutamate transporters in neurodegenerative diseases and potential opportunities for intervention.
- Amitriptyline induces nuclear transcription factor-kappaB-dependent glutamate transporter upregulation in chronic morphine-infused rats.
- Neuroprotective potential of ceftriaxone in in vitro models of stroke.
- Ifenprodil, a NR2B-selective antagonist of NMDA receptor, inhibits reverse Na+/Ca2+ exchanger in neurons
- Dopamine Regulates the Expression of the Glutamate Transporter GLT1 but Not GLAST in Developing Striatal Astrocytes
- MR relaxometry in Huntington's disease: correlation between imaging, genetic and clinical parameters.
- Targeting peroxynitrite driven nitroxidative stress with synzymes: A novel therapeutic approach in chronic pain management.
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