ArticleEndocrine1996
Adenosine 5'-triphosphate (ATP) receptors induce intracellular calcium changes in mouse leydig cells.
Article in Endocrine, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Nitric oxide modulates ATP-evoked currents in mouse Leydig cells.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2018Article
- Purinergic signaling in testes revealed.The Journal of general physiology · 2016Article
- Purinergic signaling pathways in endocrine system.Autonomic neuroscience : basic & clinical · 2015Review
- Purinergic signalling in endocrine organs.Purinergic signalling · 2014Review
- P2X receptor channels in endocrine glands.Wiley interdisciplinary reviews. Membrane transport and signaling · 2013Article
- Mouse Leydig cells express multiple P2X receptor subunits.Purinergic signalling · 2009Article
- Volume-activated chloride channels in mice Leydig cells.Pflugers Archiv : European journal of physiology · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cytoplasmic calcium ([Ca(2+)](i)) changes evoked by adenosine 5(1)-triphosphate (ATP) were recorded in cultured individual Leydig cells within 10-18 h after cell dispersion. [Ca(2+)](i) was monitored using Fura-2AM loaded cells with a digital ratio imaging system. Five micromolars ATP induced biphasic [Ca(2+)](i) responses in most cells (94%,n=100), characterized by a fast increase from a basal level (126±5 nMSE,n=60 cells) to a peak (5-7 times above basal levels) within seconds, followed by a slow decrease toward a plateau level (2-3 times above basal) within 5 min. The peak phase of the [Ca(2+)](i) response increased with ATP concentrations (1-100 μM ATP) in a dose-dependent manner with an IC(50) of 5.9±1.2 μM, and it desensitized in a reversible manner with repeated application of 5 μM ATP at <5-min intervals. The [Ca(2+)](i) peak response was dependent on Ca(2+) release from an intracellular pool, whereas the plateau phase was dependent on extracellular [Ca(2+)]. ATP did not appear to induce formation of nonspecific membrane pores, since stimulation for 10 min with ATP (10-100 μM) in the presence of extracellular Lucifer yellow (LY) (5 mg/mL) did not result in dye loading of the cells. [Ca(2+)](i) transients were elicited by other adenosine nucleotides with an order of potencies (ATP>Adenosine diphosphate [ADP]>Adenosine> Adenosine monophosphate [AMP]) that was compatible with the expression of P(2) receptors. [Ca(2+)](i) responses were suppressed by the purinergic P(2) receptor antagonist, suramin. These results provide functional evidence for the expression of purinergic P(2) receptors in Leydig cells.
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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.