ArticleBritish journal of pharmacology2004
Topiramate modulates pH of hippocampal CA3 neurons by combined effects on carbonic anhydrase and Cl-/HCO3- exchange.
Article in British journal of pharmacology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 78 citations in OpenAlex.
- Trial
- Review
- The acid-base balance homeostasis reflected by urine pH in children with infantile epileptic spasm syndrome may be associated with response to adrenocorticotropic hormone treatment: a retrospective cohort study.Translational pediatrics · 2025Article
- The Antiepileptic Drug Levetiracetam Inhibits Carbonic Anhydrase:ACS medicinal chemistry letters · 2024Article
- Synthesis, In Vivo Anticonvulsant Activity Evaluation and In Silico Studies of Some Quinazolin-4(3H)-One Derivatives.Molecules (Basel, Switzerland) · 2024Article
- Article
- A rise in saliva and urine pH in children withFrontiers in neurology · 2022Article
- The complex relationship between multiple drug resistance and the tumor pH gradient: a review.Cancer drug resistance (Alhambra, Calif.) · 2022Review
- 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
- SUNCT/SUNA in Pediatric Age: A Review of Pathophysiology and Therapeutic Options.Brain sciences · 2021Review
- Switching the Inhibitor-Enzyme Recognition Profile via Chimeric Carbonic Anhydrase XII.ChemistryOpen · 2021Article
- Deletion of the Na/HCOScientific reports · 2019Article
- Regulation of high glucose-induced apoptosis of brain pericytes by mitochondrial CA VA: A specific target for prevention of diabetic cerebrovascular pathology.Biochimica et biophysica acta. Molecular basis of disease · 2017Article
- Topiramate induces acute intracellular acidification in glioblastoma.Journal of neuro-oncology · 2016Article
- Topiramate-induced paresthesia is more frequently reported by migraine than epileptic patients.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2016Observational
- Pharmacological inhibition of mitochondrial carbonic anhydrases protects mouse cerebral pericytes from high glucose-induced oxidative stress and apoptosis.The Journal of pharmacology and experimental therapeutics · 2013Article
- Topiramate and cognitive impairment: evidence and clinical implications.Therapeutic advances in drug safety · 2012Review
- Topiramate treatment protects blood-brain barrier pericytes from hyperglycemia-induced oxidative damage in diabetic mice.Endocrinology · 2012Article
- Topiramate diminishes fear memory consolidation and extinguishes conditioned fear in rats.Journal of psychiatry & neuroscience : JPN · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Topiramate (TPM) is an anticonvulsant whose impact on firing activity and intracellular pH (pHi) regulation of CA3 neurons was investigated. Using the 4-aminopyridine-treated hippocampal slice model bathed in bicarbonate-buffered solution, TPM (25-50 microm) reduced the frequency of epileptiform bursts and action potentials without affecting membrane potential or input resistance. Inhibitory effects of TPM were reversed by trimethylamine-induced alkalinization. TPM also lowered the steady-state pHi of BCECF-AM-loaded neuronal somata by 0.18+/-0.07 pH units in CO(2)/HCO(3)(-)-buffered solution. Subsequent to an ammonium prepulse, TPM reduced the acidotic peak but clearly slowed pHi recovery. These complex changes were mimicked by the protein phosphatase inhibitor okadaic acid. Alkalosis upon withdrawal of extracellular Cl(-) was augmented by TPM. Furthermore, at decreased pHi due to the absence of extracellular Na(+), TPM reversibly increased pHi. These findings demonstrate that TPM modulates Na(+)-independent Cl(-)/HCO(3)(-) exchange. In the nominal absence of extracellular CO(2)/HCO(3)(-) buffer, both steady-state pHi and firing of epileptiform bursts remained unchanged upon adding TPM. However, pHi recovery subsequent to an ammonium prepulse was slightly increased, as was the case in the presence of the carbonic anhydrase (CA) inhibitor acetazolamide. Thus, a slight reduction of intracellular buffer capacity by TPM may be due to an inhibitory effect on intracellular CA. Together, these findings show that TPM lowers neuronal pHi most likely due to a combined effect on Na(+)-independent Cl(-)/HCO(3)(-) exchange and CA. The apparent decrease of steady-state pHi may contribute to the anticonvulsive property of TPM.
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