ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Preemptive regulation of intracellular pH in hippocampal neurons by a dual mechanism of depolarization-induced alkalinization.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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34 citing papers in PubMed, 55 citations in OpenAlex.
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- Bidirectional protein-protein interactions control liquid-liquid phase separation of PSD-95 and its interaction partners.iScience · 2022Article
- Simultaneous Monitoring of pH and Chloride (ClInternational journal of molecular sciences · 2021Article
- The accessible chromatin landscape of the murine hippocampus at single-cell resolution.Genome research · 2019Article
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- NaThe Journal of physiology · 2017Article
- Role of ClThe Journal of physiology · 2017Article
- Acute neuroinflammation provokes intracellular acidification in mouse hippocampus.Journal of neuroinflammation · 2016Article
- Modulation of Acid-sensing Ion Channel 1a by Intracellular pH and Its Role in Ischemic Stroke.The Journal of biological chemistry · 2016Article
- Acute inhibition of neurosteroid estrogen synthesis suppresses status epilepticus in an animal model.eLife · 2016Article
- Fluorescent ratiometric pH indicator SypHer2: Applications in neuroscience and regenerative biology.Biochimica et biophysica acta · 2015Article
- Phosphatidylinositol 4,5-bisphosphate degradation inhibits the Na+/bicarbonate cotransporter NBCe1-B and -C variants expressed in Xenopus oocytes.The Journal of physiology · 2015Article
- ATP binding to synaspsin IIa regulates usage and clustering of vesicles in terminals of hippocampal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Article
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4 authors at 1 institution in 1 country.
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Abstract
Numerous studies have documented the mechanisms that regulate intracellular pH (pH(i)) in hippocampal neurons in response to an acid load. Here, we studied the response of pH(i) to depolarization in cultured hippocampal neurons. Elevation of external K+ (6-30 mm) elicited an acid transient followed by a large net alkaline shift. Similar responses were observed in acutely dissociated hippocampal neurons. In Ca2+ -free media, the acid response was curtailed and the alkaline shift enhanced. DIDS blocked the alkaline response and revealed a prolonged underlying acidification that was highly dependent on Ca2+ entry. Similar alkaline responses could be elicited by AMPA, indicating that this rise in pH(i) was a depolarization-induced alkalinization (DIA). The DIA was found to consist of Cl- -dependent and Cl- -independent components, each accounting for approximately one-half of the peak amplitude. The Cl- -independent component was postulated to arise from operation of the electrogenic Na+ -HCO3- cotransporter NBCe1. Quantitative PCR and single-cell multiplex reverse transcription-PCR demonstrated message for NBCe1 in our hippocampal neurons. In neurons cultured from Slc4a4 knock-out (KO) mice, the DIA was reduced by approximately one-half compared with wild type, suggesting that NBCe1 was responsible for the Cl- -independent DIA. In Slc4a4 KO neurons, the remaining DIA was virtually abolished in Cl- -free media. These data demonstrate that DIA of hippocampal neurons occurs via NBCe1, and a parallel DIDS-sensitive, Cl- -dependent mechanism. Our results indicate that, by activating net acid extrusion in response to depolarization, hippocampal neurons can preempt a large, prolonged, Ca2+ -dependent acidosis.
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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.