ArticleJournal of neurotrauma2012
Disruptions in the regulation of extracellular glutamate by neurons and glia in the rat striatum two days after diffuse brain injury.
Article in Journal of neurotrauma, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 101 citations in OpenAlex.
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- Improving Sensitivity and Longevity of In Vivo Glutamate Sensors with Electrodeposited NanoPt.ACS applied materials & interfaces · 2024Article
- Excitotoxicity, Oxytosis/Ferroptosis, and Neurodegeneration: Emerging Insights into Mitochondrial Mechanisms.Aging and disease · 2024Review
- Epidemiology, Pathophysiology, and Treatment Strategies of Concussions: A Comprehensive Review.Fortune journal of health sciences · 2024Article
- Real-time in vivo thoracic spinal glutamate sensing during myocardial ischemia.American journal of physiology. Heart and circulatory physiology · 2023Article
- Effects of isoflurane and urethane anesthetics on glutamate neurotransmission in rat brain using in vivo amperometry.BMC neuroscience · 2023Article
- DNA Methylation-Mediated Mfn2 Gene Regulation in the Brain: A Role in Brain Trauma-Induced Mitochondrial Dysfunction and Memory Deficits.Cellular and molecular neurobiology · 2023Article
- Neuropharmacological insight into preventive intervention in posttraumatic epilepsy based on regulating glutamate homeostasis.CNS neuroscience & therapeutics · 2023Review
- Nrf2 Activation: Involvement in Central Nervous System Traumatic Injuries. A Promising Therapeutic Target of Natural Compounds.International journal of molecular sciences · 2022Review
- Astrocyte: A Foe or a Friend in Intellectual Disability-Related Diseases.Frontiers in synaptic neuroscience · 2022Review
- Differential Effects of Human P301L Tau Expression in Young versus Aged Mice.International journal of molecular sciences · 2021Article
- Building a Bridge Between NMDAR-Mediated Excitotoxicity and Mitochondrial Dysfunction in Chronic and Acute Diseases.Cellular and molecular neurobiology · 2021Review
- Cell-Based Therapies for Traumatic Brain Injury: Therapeutic Treatments and Clinical Trials.Biomedicines · 2021Review
- Traumatic Brain Injury and Stem Cells: An Overview of Clinical Trials, the Current Treatments and Future Therapeutic Approaches.Medicina (Kaunas, Lithuania) · 2020Review
- Approaches to Monitor Circuit Disruption after Traumatic Brain Injury: Frontiers in Preclinical Research.International journal of molecular sciences · 2020Review
- Secretome of Mesenchymal Stem Cells and Its Potential Protective Effects on Brain Pathologies.Molecular neurobiology · 2019Review
- Recovery of Olfactory Function After Excitotoxic Lesion of the Olfactory Bulbs Is Associated with Increases in Bulbar SIRT1 and SIRT4 Expressions.Molecular neurobiology · 2019Article
- GABAergic imbalance is normalized by dopamine DPsychopharmacology · 2019Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Disrupted regulation of extracellular glutamate in the central nervous system contributes to and can exacerbate the acute pathophysiology of traumatic brain injury (TBI). Previously, we reported increased extracellular glutamate in the striatum of anesthetized rats 2 days after diffuse brain injury. To determine the mechanism(s) responsible for increased extracellular glutamate, we used enzyme-based microelectrode arrays (MEAs) coupled with specific pharmacological agents targeted at in vivo neuronal and glial regulation of extracellular glutamate. After TBI, extracellular glutamate was significantly increased in the striatum by (∼90%) averaging 4.1±0.6 μM compared with sham 2.2±0.4 μM. Calcium-dependent neuronal glutamate release, investigated by local application of an N-type calcium channel blocker, was no longer a significant source of extracellular glutamate after TBI, compared with sham. In brain-injured animals, inhibition of glutamate uptake with local application of an excitatory amino acid transporter inhibitor produced significantly greater increase in glutamate spillover (∼ 65%) from the synapses compared with sham. Furthermore, glutamate clearance measured by locally applying glutamate into the extracellular space revealed significant reductions in glutamate clearance parameters in brain-injured animals compared with sham. Taken together, these data indicate that disruptions in calcium-mediated glutamate release and glial regulation of extracellular glutamate contribute to increased extracellular glutamate in the striatum 2 days after diffuse brain injury. Overall, these data suggest that therapeutic strategies used to regulate glutamate release and uptake may improve excitatory circuit function and, possibly, outcomes following TBI.
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