ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Synaptic acidification enhances GABAA signaling.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 69 citations in OpenAlex.
- The Proteomic Landscape of Parkin-Deficient and Parkin-Overexpressing Rat Nucleus Accumbens: An Insight into the Role of Parkin in Methamphetamine Use Disorder.Biomolecules · 2025Article
- A pH-sensitive closed-loop nanomachine to control hyperexcitability at the single neuron level.Nature communications · 2024Article
- Spreading depolarizations pose critical energy challenges in acute brain injury.Journal of neurochemistry · 2024Review
- The role of NaPflugers Archiv : European journal of physiology · 2024Review
- The Systemic Administration of NaJournal of clinical practice and research · 2024Article
- SLC4A10 mutation causes a neurological disorder associated with impaired GABAergic transmission.Brain : a journal of neurology · 2023Article
- Triggering of Major Brain Disorders by Protons and ATP: The Role of ASICs and P2X Receptors.Neuroscience bulletin · 2023Review
- Upregulation of carbonic anhydrase 1 beneficial for depressive disorder.Acta neuropathologica communications · 2023Article
- Stress-induced reduction of NaScience advances · 2022Article
- Roles of Endomembrane Alkali Cation/Proton Exchangers in Synaptic Function and Neurodevelopmental Disorders.Frontiers in physiology · 2022Review
- αACS chemical neuroscience · 2021Article
- Neurodegenerative Disease: What Potential Therapeutic Role of Acid-Sensing Ion Channels?Frontiers in cellular neuroscience · 2021Review
- Acid-Sensing Ion Channels: Focus on Physiological and Some Pathological Roles in the Brain.Current neuropharmacology · 2021Review
- The Classification of Autosomal Recessive Cerebellar Ataxias: a Consensus Statement from the Society for Research on the Cerebellum and Ataxias Task Force.Cerebellum (London, England) · 2019Review
- Intracellular pH Regulation in iPSCs-derived Astrocytes from Subjects with Chronic Mountain Sickness.Neuroscience · 2018Article
- Protons as Messengers of Intercellular Communication in the Nervous System.Frontiers in cellular neuroscience · 2018Review
- Deactivation kinetics of acid-sensing ion channel 1a are strongly pH-sensitive.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Acute neuroinflammation provokes intracellular acidification in mouse hippocampus.Journal of neuroinflammation · 2016Article
- A modulatory role of ASICs on GABAergic synapses in rat hippocampal cell cultures.Molecular brain · 2016Article
- The function and regulation of acid-sensing ion channels (ASICs) and the epithelial Na(+) channel (ENaC): IUPHAR Review 19.British journal of pharmacology · 2016Review
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
To determine the role of cellularly generated protons in synaptic signaling, we recorded GABA miniature IPSCs (mIPSCs) from cultured rat cerebellar granule cells (CGCs) while varying the extracellular pH buffering capacity. Consistent with previous reports, we found that increasing pH from 7.4 to 8.0 sped mIPSC rise time and suppressed both amplitude of the current and total charge transferred. Conversely, acidification (from pH 7.4 to 6.8) slowed the rise time and increased current amplitude and total charge transferred. In a manner consistent with alkalinization, increasing the buffering capacity from 3 to 24 mm HEPES at pH 7.4 resulted in faster mIPSC rise time, a 37% reduction in amplitude, and a 48% reduction in charge transferred. Supplementing the normal physiological buffers (24 mm HCO(3)(-)/5%CO(2)) with 10 mm HEPES similarly diminished mIPSCs in a manner consistent with alkalinization, resulting in faster rise time, a 39% reduction in amplitude, and a 51% reduction in charge transferred. These findings suggest the existence of an acidifying synaptic force that is overcome by commonly used concentrations (10 mm) of HEPES buffer. Here we show that Na(+)/H(+) exchanger (NHE) activity appears to, in part, contribute to this synaptic acidification because inhibition of NHE by amiloride or lithium under physiological or weak buffering conditions alters mIPSCs in a manner consistent with alkalinization. These results suggest that acidification of the synaptic cleft occurs physiologically during GABAergic transmission and that NHE plays a critical role in generating the acidic nano-environment at the synapse.
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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.