Linked Life Data

11108818

Source:http://linkedlifedata.com/resource/pubmed/id/11108818

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pubmed-article:11108818pubmed:abstractTextElectrophysiological and Ca2+ microfluorimetric techniques were used to characterize the pharmacological profile of the P2 receptors expressed in submucosal neurons and the changes in intracellular Ca2+ associated with activation of these receptors. ATP caused a fast and slow membrane depolarizations during intracellular recordings. ATP induced a rapid inward current during whole-cell experiments. Receptors mediating the inward current and fast depolarization have the same pharmacological profile and these ATP responses were more sensitive to pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid than Basilen BlueE-3G, and potentiated by suramin. The slow depolarization was not blocked by these P2 receptor antagonists, pertussis toxin, or KT5720 (protein kinase A inhibitor). N-ethylmaleimide or protein kinase C inhibitors (staurosporine and calphostin) blocked this depolarization. ATP induced complex multi-phasic Ca2+ transients in most neurons, classified as fast, slow, or mixed fast/slow responses. In conclusion, the fast and slow Ca2+ responses were mediated by respective activation of P2X and P2Y receptors and were associated with fast and slow depolarizations, respectively.lld:pubmed
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pubmed-article:11108818pubmed:pagination243-57lld:pubmed
pubmed-article:11108818pubmed:dateRevised2010-11-18lld:pubmed
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pubmed-article:11108818pubmed:articleTitleChanges in intracellular Ca2+ by activation of P2 receptors in submucosal neurons in short-term cultures.lld:pubmed
pubmed-article:11108818pubmed:affiliationDepartment of Anatomy and Cell Biology, Queen's University, 9th Floor Botterell Hall, Kingston, ON K7L3N6, Canada. barajasc@meds.queensu.calld:pubmed
pubmed-article:11108818pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:11108818pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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