ArticleThe Journal of physiology2003
Acidosis decreases low Ca(2+)-induced neuronal excitation by inhibiting the activity of calcium-sensing cation channels in cultured mouse hippocampal neurons.
Article in The Journal of physiology, 2003. 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, 32 citations in OpenAlex.
- The background sodium leak channel NALCN is a major controlling factor in pituitary cell excitability.The Journal of physiology · 2025Article
- The effect of diminished metabolic acidosis on thermoregulatory response during exercise.Biology of sport · 2024Article
- CaInternational journal of molecular sciences · 2022Review
- GeLife · 2018Article
- Modulation of Human Cardiac TRPM7 Current by Extracellular Acidic pH Depends upon Extracellular Concentrations of Divalent Cations.PloS one · 2017Article
- The function and regulation of acid-sensing ion channels (ASICs) and the epithelial Na(+) channel (ENaC): IUPHAR Review 19.British journal of pharmacology · 2016Review
- Modulation of Acid-sensing Ion Channel 1a by Intracellular pH and Its Role in Ischemic Stroke.The Journal of biological chemistry · 2016Article
- Extracellular spermine exacerbates ischemic neuronal injury through sensitization of ASIC1a channels to extracellular acidosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Modulation of acid-sensing ion channels: molecular mechanisms and therapeutic potential.International journal of physiology, pathophysiology and pharmacology · 2011Article
- The modulation of TRPM7 currents by nafamostat mesilate depends directly upon extracellular concentrations of divalent cations.Molecular brain · 2010Article
- Calcium sensitive non-selective cation current promotes seizure-like discharges and spreading depression in a model neuron.Journal of computational neuroscience · 2009Article
- Mechanisms underlying low [Ca(2+)](o)-induced increased excitability of hippocampal neurons.Neuroscience bulletin · 2008Article
- TRPM7 channels in hippocampal neurons detect levels of extracellular divalent cations.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Emergence of a spermine-sensitive, non-inactivating conductance in mature hippocampal CA1 pyramidal neurons upon reduction of extracellular Ca2+: dependence on intracellular Mg2+ and ATP.Neurochemistry international · 2007Article
- Subunit-dependent high-affinity zinc inhibition of acid-sensing ion channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- Magnesium-inhibited, TRPM6/7-like channel in cardiac myocytes: permeation of divalent cations and pH-mediated regulation.The Journal of physiology · 2004Article
- Effects of lactate and carbon monoxide interactions on neuroprotection and neuropreservation.Medical gas researchArticle
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The effects of extracellular pH (pHo) on calcium-sensing non-selective cation (csNSC) channels in cultured mouse hippocampal neurons were investigated using whole-cell voltage-clamp and current-clamp recordings. Decreasing extracellular Ca2+ concentrations ([Ca2+]o) activated slow and sustained inward currents through the csNSC channels. Decreasing pHo activated amiloride-sensitive transient proton-gated currents which decayed to baseline in several seconds. With proton-gated channels inactivated by pre-perfusion with low pH solution or blocked by amiloride, decreasing pHo to 6.5 inhibited the csNSC currents with a leftward shift of the Ca2+ dose-inhibition curve. Increasing pH to 8.5, on the other hand, caused a rightward shift of the Ca2+ dose-inhibition curve and potentiated the csNSC currents. Intracellular alkalinization following bath perfusion of quinine mimicked the potentiation of the csNSC currents by increasing pHo, while intracellular acidification by addition and subsequent withdrawal of NH4Cl mimicked the inhibition of the csNSC currents by decreasing pHo. Intracellular pH (pHi) imaging demonstrated that decreasing pHo induced a corresponding decrease in pHi. Including 30 mM Hepes in the pipette solution eliminated the effects of quinine and NH4Cl on the csNSC currents, but only partially reduced the effect of lowering pHo. In current-clamp recordings, decreasing [Ca2+]o induced sustained membrane depolarization and excitation of hippocampal neurons. Decreasing pHo to 6.5 inhibited the low [Ca2+]o-induced csNSC channel-mediated membrane depolarization and the excitation of neurons. Our results indicate that acidosis may inhibit low [Ca2+]o-induced neuronal excitation by inhibiting the activity of the csNSC channels. Both the extracellular and the intracellular sites are involved in the proton modulation of the csNSC channels.
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