ArticleThe Journal of physiology2004
Quantal release of ATP from clusters of PC12 cells.
Article in The Journal of physiology, 2004. 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, 39 citations in OpenAlex.
- Released ATP Mediates Spermatozoa Chemotaxis Promoted by Uterus-Derived Factor (UDF) inInternational journal of molecular sciences · 2022Article
- Tonic Calcium-Activated Chloride Current Sustained by ATP Release and Highly Desensitizing Human P2X1 Receptors.Neuroscience · 2020Article
- Extracellular Nucleotides and P2 Receptors in Renal Function.Physiological reviews · 2020Review
- Nicotine protects rat hypoglossal motoneurons from excitotoxic death via downregulation of connexin 36.Cell death & disease · 2017Article
- Nucleotide homeostasis and purinergic nociceptive signaling in rat meninges in migraine-like conditions.Purinergic signalling · 2016Article
- The purinergic neurotransmitter revisited: a single substance or multiple players?Pharmacology & therapeutics · 2014Review
- Purinergic signaling in early inflammatory events of the foreign body response: modulating extracellular ATP as an enabling technology for engineered implants and tissues.Tissue engineering. Part B, Reviews · 2014Review
- Purinergic signalling and cancer.Purinergic signalling · 2013Review
- Purinergic signaling in inflammatory renal disease.Frontiers in physiology · 2013Article
- The expression level of ecto-NTP diphosphohydrolase1/CD39 modulates exocytotic and ischemic release of neurotransmitters in a cellular model of sympathetic neurons.The Journal of pharmacology and experimental therapeutics · 2011Article
- P2X7 receptors trigger ATP exocytosis and modify secretory vesicle dynamics in neuroblastoma cells.The Journal of biological chemistry · 2011Article
- Complex role of zinc in methamphetamine toxicity in vitro.Neuroscience · 2010Article
- ATP release from non-excitable cells.Purinergic signalling · 2009Article
- Identification of a vesicular nucleotide transporter.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Vesicular release of ATP at central synapses.Pflugers Archiv : European journal of physiology · 2006Review
- Glutamate uptake block triggers deadly rhythmic bursting of neonatal rat hypoglossal motoneurons.The Journal of physiology · 2006Article
- Basal activation of the P2X7 ATP receptor elevates mitochondrial calcium and potential, increases cellular ATP levels, and promotes serum-independent growth.Molecular biology of the cell · 2005Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although ATP is important for intercellular communication, little is known about the mechanism of endogenous ATP release due to a dearth of suitable models. Using PC12 cells known to express the P2X2 subtype of ATP receptors and to store ATP with catecholamines inside dense-core vesicles, we found that clusters of PC12 cells cultured for 3-7 days generated small transient inward currents (STICs) after an inward current elicited by exogenous ATP. The amplitude of STICs in individual cells correlated with the peak amplitude of ATP-induced currents. STICs appeared as asynchronous responses (approximately 20 pA average amplitude) for 1-20 s and were investigated with a combination of patch clamping, Ca2+ imaging, biochemistry and electron microscopy. Comparable STICs were produced by focal KCl pulses and were dependent on extracellular Ca2+. STICs were abolished by the P2X antagonist PPADS and potentiated by Zn2+, suggesting they were mediated by P2X2 receptor activation. The highest probability of observing STICs was after the peak of intracellular Ca2+ increase caused by KCl. Biochemical measurements indicated that KCl application induced a significant release of ATP from PC12 cells. Electron microscopy studies showed narrow clefts without 'synaptic-like' densities between clustered cells. Our data suggest that STICs were caused by quantal release of endogenous ATP by depolarized PC12 cells in close juxtaposition to the recorded cell. Thus, STICs may be a new experimental model to characterize the physiology of vesicular release of ATP and to study the kinetics and pharmacology of P2X2 receptor-mediated quantal currents.
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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.