ArticlePloS one2017
Faster flux of neurotransmitter glutamate during seizure - Evidence from 13C-enrichment of extracellular glutamate in kainate rat model.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 15 citations in OpenAlex.
- Detection of regional metabolic alteration using 7T deuterium metabolic imaging in MRI-negative,Magma (New York, N.Y.) · 2026Article
- Modern Analytical Techniques in Epilepsy Research.International journal of molecular sciences · 2026Review
- Role of hippocampus in epileptogenesis: new insights in the cross-talks between the underlying mechanisms.Acta neurologica Belgica · 2025Review
- Excitotoxic glutamate levels cause the secretion of resident endoplasmic reticulum proteins.Journal of neurochemistry · 2024Article
- Microdialysis and microperfusion electrodes in neurologic disease monitoring.Fluids and barriers of the CNS · 2021Review
- Astrocyte Glutamate Uptake and Signaling as Novel Targets for Antiepileptogenic Therapy.Frontiers in neurology · 2020Review
- Ephrin‑b3 modulates hippocampal neurogenesis and the reelin signaling pathway in a pilocarpine‑induced model of epilepsy.International journal of molecular medicine · 2018Article
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Abstract
The objective is to examine how the flux of neurotransmitter glutamate from neurons to the extracellular fluid, as measured by the rate of 13C enrichment of extracellular glutamate (GLUECF), changes in response to seizures in the kainate-induced rat model of temporal-lobe epilepsy. Following unilateral intrahippocampal injection of kainate, GLUECF was collected by microdialysis from the CA1/CA3 region of awake rats, in combination with EEG recording of chronic-phase recurrent seizures and intravenous infusion of [2,5-13C]glucose. The 13C enrichment of GLUECF C5 at ~ 10 picomol level was measured by gas-chromatography mass-spectrometry. The rate of 13C enrichment, expressed as the increase of the fractional enrichment/min, was 0.0029 ± 0.0001/min in frequently seizing rats (n = 4); this was significantly higher (p < 0.01) than in the control (0.00167 ± 0.0001/min; n = 6) or in rats with infrequent seizures (0.00172 ± 0.0001/min; n = 6). This result strongly suggests that the flux of the excitatory neurotransmitter from neurons to the extracellular fluid is significantly increased by frequent seizures. The extracellular [12C + 13C]glutamate concentration increased progressively in frequently seizing rats. Taken together, these results strongly suggest that the observed seizure-induced high flux of glutamate overstimulated glutamate receptors, which triggered a chain reaction of excitation in the CA3 recurrent glutamatergic networks. The rate of 13C enrichment of extracellular glutamine (GLNECF) at C5 was 0.00299 ± 0.00027/min in frequently seizing rats, which was higher (p < 0.05) than in controls (0.00227 ± 0.00008/min). For the first time in vivo, this study examined the effects of epileptic seizures on fluxes of the neurotransmitter glutamate and its precursor glutamine in the extracellular fluid of the hippocampus. The advantages, limitations and the potential for improvement of this approach for pre-clinical and clinical studies of temporal-lobe epilepsy are discussed.
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