ReviewNeurochemical research2017
Mechanisms of Excessive Extracellular Glutamate Accumulation in Temporal Lobe Epilepsy.
Review in Neurochemical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 75 citations in OpenAlex.
- Anti-Inflammatory and Antioxidant Strategies in Epilepsy: From Molecular Mechanisms to Threshold Management.International journal of molecular sciences · 2026Review
- Epilepsy: Molecular Pathogenesis and Emerging Therapies.MedComm · 2026Review
- From gut to brain: short-term ketogenic diet alleviates status epilepticus-induced cognitive deficits in rats.Frontiers in physiology · 2026Article
- Ethnopharmacological relevance of Chinese medicinal materials and natural products in epilepsy: a critical multi-target review integrating neurons, glia and inflammatory signaling.Frontiers in pharmacology · 2026Review
- Effects and Mechanisms of NMDAR-EphB2 on Synapses in Mice by Active Immunization with a GluN1 Peptide.Molecular neurobiology · 2025Article
- WONOEP XVII appraisal: Targeting network excitability beyond the synapse -Neurotransmitter, ionic, and electro -diffusions.Epilepsia · 2025Review
- KMO Inhibition Improves Seizures and Depressive-like Behaviors Without Aggravating Cognitive Impairment in Epileptic Mice.Current issues in molecular biology · 2025Article
- Review
- Excitatory Amino Acid Transporters as Therapeutic Targets in the Treatment of Neurological Disorders: Their Roles and Therapeutic Prospects.Neurochemical research · 2025Review
- Ferroptosis and epilepsy: bidirectional pathogenic links and therapeutic implications.Frontiers in neurology · 2025Review
- Anticonvulsive Effect of Glucosyl Xanthone Mangiferin on Pentylenetetrazol (PTZ)-Induced Seizure-Provoked Mice.Applied biochemistry and biotechnology · 2024Article
- The role of extracellular glutamate homeostasis dysregulated by astrocyte in epileptic discharges: a model evidence.Cognitive neurodynamics · 2024Article
- Article
- Acute activation of hemichannels by ethanol leads to CaFrontiers in cell and developmental biology · 2024Article
- Efficacy of Personalized Postoperative Epilepsy Management in Patients with Glioblastoma Utilizing IDH1 Gene Assessment.Neuropsychiatric disease and treatment · 2024Article
- Latest advances in mechanisms of epileptic activity in Alzheimer's disease and dementia with Lewy Bodies.Frontiers in neurology · 2024Review
- The Interplay between Mitochondrial Dysfunction and Ferroptosis during Ischemia-Associated Central Nervous System Diseases.Brain sciences · 2023Review
- Clinical Improvement in Depression and Cognitive Deficit Following Electroconvulsive Therapy.Diagnostics (Basel, Switzerland) · 2023Review
- Role of long noncoding RNAs; BDNF-AS and 17A and their relation to GABAergic dysfunction in Egyptian epileptic patients.Metabolic brain disease · 2023Article
- γ-Aminobutyric acid as a biomarker of the lateralizing and monitoring drug effect in patients with magnetic resonance imaging-negative temporal lobe epilepsy.Frontiers in neuroscience · 2023Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There is compelling evidence that initiation and maintenance of epileptic seizures in temporal lobe epilepsy (TLE) is facilitated by excessive accumulation in the extracellular (perisynaptic) space of the excitatory neurotransmitter glutamate (Glu). This review discusses the mechanisms underlying this phenomenon. Glu released from neurons is taken up by astrocytes and activated there by glutamine synthetase (GS) to form glutamine (Gln) which upon entry to neurons is degraded back to Glu by phosphate-activated glutaminase (PAG): this chain of reactions has been defined as the glutamine/glutamate/cycle (GGC). In the initial phase of epileptogenesis, increased Glu supply is a consequence of activation of its turnover in GGC by Glu released by a primary chemical or physical stimulus. In chronic TLE, profound astrogliosis and demise of neurons which culminate in hippocampal sclerosis, are associated with changes in GGC which act in concert towards increasing the extracellular Glu concentration. Deficiency of GS and of the astrocytic Glu transporter, GLT-1, impede Glu inactivation, whereas Glu release from neurons appears facilitated by activation of PAG and increased activity of the neuronal Glu transporter EAAC1. Conclusions derived from measurements of activities/expression patterns of the GGC enzymes and transporter moieties find support in metabolic studies employing
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