ArticleEpilepsia2013
Down-regulation of gephyrin and GABAA receptor subunits during epileptogenesis in the CA1 region of hippocampus.
Article in Epilepsia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 42 citations in OpenAlex.
- GABASynapse (New York, N.Y.) · 2026Review
- GABACellular and molecular neurobiology · 2026Review
- Induced epileptic seizures in larval zebrafish reveal a synaptic modulation associated with the post-ictal state.Brain communications · 2026Article
- Review
- Clptm1, a new target in suppressing epileptic seizure by regulating GABAThe Kaohsiung journal of medical sciences · 2023Article
- Regulation of Inhibitory Signaling at the Receptor and Cellular Level; Advances in Our Understanding of GABAergic Neurotransmission and the Mechanisms by Which It Is Disrupted in Epilepsy.Frontiers in synaptic neuroscience · 2022Review
- Divergent metabolic substrate utilization in brain during epileptogenesis precedes chronic hypometabolism.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020Article
- Calpain-dependent cleavage of GABAergic proteins during epileptogenesis.Epilepsy research · 2019Article
- Calpain activation and neuronal death during early epileptogenesis.Neurobiology of disease · 2019Article
- Neurosteroid regulation of GABABrain research · 2019Review
- Rare Variants in 48 Genes Account for 42% of Cases of Epilepsy With or Without Neurodevelopmental Delay in 246 Pediatric Patients.Frontiers in neuroscience · 2019Article
- Diazepam Accelerates GABAFrontiers in cellular neuroscience · 2019Article
- Alterations in GABAFrontiers in cellular neuroscience · 2019Article
- Gephyrin: a key regulatory protein of inhibitory synapses and beyond.Histochemistry and cell biology · 2018Review
- Oxytocin and vasopressin modulation of social anxiety following adolescent intermittent ethanol exposure.Psychopharmacology · 2018Article
- The adjustment of γ-aminobutyric acidNeural regeneration research · 2018Review
- The Effects of Ginsenoside Compound K Against Epilepsy by Enhancing the γ-Aminobutyric Acid Signaling Pathway.Frontiers in pharmacology · 2018Article
- Neurosteroid-sensitive δ-GABAEpilepsia · 2017Article
- Regulation of the cell surface expression of chloride transporters during epileptogenesis.Neuroscience letters · 2016Article
- Gephyrin Cleavage in In Vitro Brain Ischemia Decreases GABAA Receptor Clustering and Contributes to Neuronal Death.Molecular neurobiology · 2016Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
purposeEpileptogenesis is the process by which a brain becomes hyperexcitable and capable of generating recurrent spontaneous seizures. In humans, it has been hypothesized that following a brain insult there are a number of molecular and cellular changes that underlie the development of spontaneous seizures. Studies in animal models have shown that an injured brain may develop epileptiform activity before appearance of epileptic seizures and that the pathophysiology accompanying spontaneous seizures is associated with a dysfunction of γ-aminobutyric acid (GABA)ergic neurotransmission. Here, we analyzed the effects of status epilepticus on the expression of GABAA receptors (GABAA Rs) and scaffolding proteins involved in the regulation of GABAA R trafficking and anchoring.
methodsWestern blot analysis was used to determine the levels of proteins involved in GABAA R trafficking and anchoring in adult rats subjected to pilocarpine-induced status epilepticus (SE) and controls. Cell surface biotinylation using a cell membrane-impermeable reagent was used to assay for changes in the expression of receptors at the plasma membrane. Finally, immunoprecipitation experiments were used to evaluate the composition of GABAA Rs. We examined for a correlation between total GABAA R subunit expression, plasma membrane expression, and receptor composition. KEY
findingsAnalysis of tissue samples from the CA1 region of hippocampus show that SE promotes a loss of GABAA R subunits and of the scaffolding proteins associated with them. We also found a decrease in the levels of receptors located at the plasma membrane and alterations in GABAA R composition. SIGNIFICANCE: The changes in protein expression of GABAA Rs and scaffolding proteins detected in these studies provide a potential mechanism to explain the deficits in GABAergic neurotransmission observed during the epileptogenic period. Our current observations represent an additional step toward the elucidation of the molecular mechanisms underlying GABAA R dysfunction during epileptogenesis.
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