ArticleNeuropharmacology2015
Carbonic anhydrase inhibition by acetazolamide reduces in vitro epileptiform synchronization.
Article in Neuropharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 34 citations in OpenAlex.
- The Protective Role of Aquaporin 4 (AQP4) in Temporal Lobe Epilepsy: Yes or No?Journal of molecular neuroscience : MN · 2026Review
- Applications of Carbonic Anhydrase Inhibitors in Neurological Disorders, Mechanisms and Therapeutic Potential.Sub-cellular biochemistry · 2026Review
- Direct energy consumption by inhibitory GABAFrontiers in neuroscience · 2026Article
- Neurovascular coupling is optimized to compensate for the increase in proton production from nonoxidative glycolysis and glycogenolysis during brain activation and maintain homeostasis of pH, pCOJournal of neurochemistry · 2024Article
- Acetazolamide: Old drug, new evidence?Epilepsia open · 2022Review
- High-Frequency Oscillations and Epileptogenic Network.Current neuropharmacology · 2022Article
- Anticonvulsant Effects of Carbonic Anhydrase Inhibitors: The Enigmatic Link Between Carbonic Anhydrases and Electrical Activity of the Brain.Neurochemical research · 2021Review
- Carbonic Anhydrase Inhibitors and Epilepsy: State of the Art and Future Perspectives.Molecules (Basel, Switzerland) · 2021Review
- Dysregulation of GABAergic Signaling in Neurodevelomental Disorders: Targeting Cation-Chloride Co-transporters to Re-establish a Proper E/I Balance.Frontiers in cellular neuroscience · 2021Review
- A Novel Sulfonamide, 4-FS, Reduces Ethanol Drinking and Physical Withdrawal Associated With Ethanol Dependence.International journal of molecular sciences · 2020Article
- Characterization of Carbonic Anhydrase In Vivo Using Magnetic Resonance Spectroscopy.International journal of molecular sciences · 2020Review
- Cognitive impairment after traumatic brain injury is associated with reduced long-term depression of excitatory postsynaptic potential in the rat hippocampal dentate gyrus.Neural regeneration research · 2018Article
- Epidemiology of traumatic brain injury-associated epilepsy and early use of anti-epilepsy drugs: An analysis of insurance claims data, 2004-2014.Epilepsy research · 2018Article
- Bicarbonate directly modulates activity of chemosensitive neurons in the retrotrapezoid nucleus.The Journal of physiology · 2018Article
- Acetazolamide potentiates the afferent drive to prefrontal cortex in vivo.Physiological reports · 2017Article
- Phenols and Polyphenols as Carbonic Anhydrase Inhibitors.Molecules (Basel, Switzerland) · 2016Review
- Emerging roles of Na⁺/H⁺ exchangers in epilepsy and developmental brain disorders.Progress in neurobiologyReview
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Depolarizing GABAA receptor-mediated currents are contributed by HCO3(-) efflux, and play a role in initiating ictal-like epileptiform events in several cortical structures supporting the view that GABAA receptor signaling actively participates to epileptiform synchronization. We employed here field potential recordings to analyze the effects of the carbonic anhydrase inhibitor acetazolamide (10 μM) on the epileptiform activity generated in vitro by piriform and entorhinal cortices (PC and EC, respectively) during application of the K(+) channel blocker 4-aminopyridine (4AP, 50 μM). Under these experimental conditions ictal- and interictal-like discharges along with high-frequency oscillations (ripples: 80-200 Hz, fast ripples: 250-500 Hz) occurred in these two regions. In both PC and EC, acetazolamide: (i) reduced the duration and the interval of occurrence of ictal discharges along with the associated ripples and fast ripples; (ii) decreased the interval of occurrence of interictal discharges and the rates of associated fast ripples; and (iii) diminished the duration and amplitude of pharmacologically isolated GABAergic events while increasing their interval of occurrence. Our results indicate that acetazolamide effectively controls 4AP-induced epileptiform synchronization in PC and EC. We propose that this action may rest on decreased GABAA receptor-mediated HCO3(-) efflux leading to diminished depolarization of principal cells and, perhaps, of interneurons.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.