ArticleProceedings of the National Academy of Sciences of the United States of America2001
Local uncaging of caged Ca(2+) reveals distribution of Ca(2+)-activated Cl(-) channels in pancreatic acinar cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 102 citations in OpenAlex.
- Pancreatic acinar cell signalling and function exhibit an absolute requirement for activation of GαThe Journal of physiology · 2025Article
- Neuronal and hormonal control of CaThe Journal of physiology · 2024Review
- Multifaceted mitochondria: moving mitochondrial science beyond function and dysfunction.Nature metabolism · 2023Review
- Watching Living Cells in Action in the Exocrine Pancreas: The Palade Prize Lecture.Function (Oxford, England) · 2023Review
- Electrophysiology of Exocrine Gland Cells.Bioelectricity · 2022Article
- CaCold Spring Harbor perspectives in biology · 2020Review
- Ion Channel Signature in Healthy Pancreas and Pancreatic Ductal Adenocarcinoma.Frontiers in pharmacology · 2020Review
- ClAmerican journal of physiology. Cell physiology · 2020Review
- Anoctamin 8 tethers endoplasmic reticulum and plasma membrane for assembly of CaThe EMBO journal · 2019Article
- New saliva secretion model based on the expression of NaPflugers Archiv : European journal of physiology · 2018Article
- CaThe Journal of physiology · 2017Review
- Orai1 and STIM1 in ER/PM junctions: roles in pancreatic cell function and dysfunction.American journal of physiology. Cell physiology · 2016Review
- Ca(2+) signals mediated by bradykinin type 2 receptors in normal pancreatic stellate cells can be inhibited by specific Ca(2+) channel blockade.The Journal of physiology · 2016Article
- The role of Ca2+ in the pathophysiology of pancreatitis.The Journal of physiology · 2014Review
- Specific mitochondrial functions in separate sub-cellular domains of pancreatic acinar cells.Pflugers Archiv : European journal of physiology · 2012Review
- Apical Ca2+-activated potassium channels in mouse parotid acinar cells.The Journal of general physiology · 2012Article
- International Union of Basic and Clinical Pharmacology. LXXXV: calcium-activated chloride channels.Pharmacological reviews · 2012Review
- A mathematical model of fluid secretion from a parotid acinar cell.Journal of theoretical biology · 2007Article
- From Galvani to patch clamp: the development of electrophysiology.Pflugers Archiv : European journal of physiology · 2006Article
- Calcium-dependent release of NO from intracellular S-nitrosothiols.The EMBO journal · 2006Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In exocrine acinar cells, Ca(2+)-activated Cl(-) channels in the apical membrane are essential for fluid secretion, but it is unclear whether such channels are important for Cl(-) uptake at the base. Whole-cell current recording, combined with local uncaging of caged Ca(2+), was used to reveal the Cl(-) channel distribution in mouse pancreatic acinar cells, where approximately 90% of the current activated by Ca(2+) in response to acetylcholine was carried by Cl(-). When caged Ca(2+) in the cytosol was uncaged locally in the apical pole, the Cl(-) current was activated, whereas local Ca(2+) uncaging in the basal or lateral areas of the cell had no effect. Even when Ca(2+) was uncaged along the whole inner surface of the basolateral membrane, no Cl(-) current was elicited. There was little current deactivation at a high cytosolic Ca(2+) concentration ([Ca(2+)](c)), but at a low [Ca(2+)](c) there was clear voltage-dependent deactivation, which increased with hyperpolarization. Functional Ca(2+)-activated Cl(-) channels are expressed exclusively in the apical membrane and channel opening is strictly regulated by [Ca(2+)](c) and membrane potential. Ca(2+)-activated Cl(-) channels do not mediate Cl(-) uptake at the base, but acetylcholine-elicited local [Ca(2+)](c) spiking in the apical pole can regulate fluid secretion by controlling the opening of these channels in the apical membrane.
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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.