ArticleJournal of biomedical science2012
Rapid compensatory changes in the expression of EAAT-3 and GAT-1 transporters during seizures in cells of the CA1 and dentate gyrus.
Article in Journal of biomedical science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 20 citations in OpenAlex.
- Moxibustion pre-treatment attenuates seizure severity during status epilepticus and counteracts the proconvulsant function of the purinergic P2X7 receptor.Purinergic signalling · 2025Article
- Selective modulation of epileptic tissue by an adenosine ABritish journal of pharmacology · 2024Article
- Influence of glutamate and GABA transport on brain excitatory/inhibitory balance.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- Transient Morphological Alterations in the Hippocampus After Pentylenetetrazole-Induced Seizures in Rats.Neurochemical research · 2018Article
- NKCC1 up-regulation contributes to early post-traumatic seizures and increased post-traumatic seizure susceptibility.Brain structure & function · 2017Article
- Early morphological and functional changes in the GABAergic system of hippocampus in the rat lithium-pilocarpine model of epilepsy.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections · 2017Article
- The importance of the excitatory amino acid transporter 3 (EAAT3).Neurochemistry international · 2016Review
- Intermittent hypoxia preconditioning-induced epileptic tolerance by upregulation of monocarboxylate transporter 4 expression in rat hippocampal astrocytes.Neurochemical research · 2014Article
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4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundEpilepsy is a neurological disorder produced by an imbalance between excitatory and inhibitory neurotransmission, in which transporters of both glutamate and GABA have been implicated. Hence, at different times after local administration of the convulsive drug 4-aminopyridine (4-AP) we analyzed the expression of EAAT-3 and GAT-1 transporter proteins in cells of the CA1 and dentate gyrus.
methodsDual immunofluorescence was used to detect the co-localization of transporters and a neuronal marker. In parallel, EEG recordings were performed and convulsive behavior was rated using a modified Racine Scale.
resultsBy 60 min after 4-AP injection, EAAT-3/NeuN co-labelling had increased in dentate granule cells and decreased in CA1 pyramidal cells. In the latter, this decrease persisted for up to 180 min after 4-AP administration. In both the DG and CA1, the number of GAT-1 labeled cells increased 60 min after 4-AP administration, although by 180 min GAT-1 labeled cells decreased in the DG alone. The increase in EAAT-3/NeuN colabelling in DG was correlated with maximum epileptiform activity and convulsive behavior.
conclusionsThese findings suggest that a compensatory mechanism exists to protect against acute seizures induced by 4-AP, whereby EAAT-3/NeuN cells is rapidly up regulated in order to enhance the removal of glutamate from the extrasynaptic space, and attenuating seizure activity.
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