title: Sodium/calcium exchangers selectively regulate calcium signaling in mouse taste receptor cells.
abstract: Taste cells use multiple signaling mechanisms to generate appropriate cellular responses to discrete taste stimuli. Some taste stimuli activate G protein coupled receptors (GPCRs) that cause calcium release from intracellular stores while other stimuli depolarize taste cells to cause calcium influx through voltage-gated calcium channels (VGCCs). While the signaling mechanisms that initiate calcium signals have been described in taste cells, the calcium clearance mechanisms (CCMs) that contribute to the termination of these signals have not been identified. In this study, we used calcium imaging to define the role of sodium-calcium exchangers (NCXs) in the termination of evoked calcium responses. We found that NCXs regulate the calcium signals that rely on calcium influx at the plasma membrane but do not significantly contribute to the calcium signals that depend on calcium release from internal stores. Our data indicate that this selective regulation of calcium signals by NCXs is due primarily to their location in the cell rather than to the differences in cytosolic calcium loads. This is the first report to define the physiological role for any of the CCMs utilized by taste cells to regulate their evoked calcium responses.
authors.affiliation: Department of Biological Sciences, University at Buffalo, The State University of New York, Buffalo, New York 14260, USA.
authors.forename: Steven A
authors.initials: SA
authors.lastname: Szebenyi
authors.forename: Agnieszka I
authors.initials: AI
authors.lastname: Laskowski
authors.forename: Kathryn F
authors.initials: KF
authors.lastname: Medler
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism; D015220:Calcium Channels / Q000187:drug effects; D020013:Calcium Signaling / Q000502:physiology*; D005071:Evoked Potentials / Q000502:physiology; D066298:In Vitro Techniques; D015640:Ion Channel Gating / Q000187:drug effects; D008094:Lithium / Q000494:pharmacology; D051379:Mice; D008810:Mice, Inbred C57BL; D043562:Receptors, G-Protein-Coupled / Q000502:physiology; D012964:Sodium / Q000494:pharmacology; D019831:Sodium-Calcium Exchanger / Q000037:antagonists & inhibitors / Q000502:physiology*; D013649:Taste / Q000502:physiology*; D013650:Taste Buds / Q000502:physiology*
chemical_list: D015220:Calcium Channels; D043562:Receptors, G-Protein-Coupled; D019831:Sodium-Calcium Exchanger; D008094:Lithium; D012964:Sodium; D002118:Calcium
references.citation: Neuron. 2003 Oct 9;40(2):331-46
references.pmid: 14556712
references.citation: EMBO J. 2007 Feb 7;26(3):657-67
references.pmid: 17235286
references.citation: Nature. 1998 Oct 15;395(6703):645-8
references.pmid: 9790183
references.citation: BMC Biol. 2006 Mar 30;4:7
references.pmid: 16573824
references.citation: J Gen Physiol. 2008 Dec;132(6):731-44
references.pmid: 19029378
references.citation: J Neurosci. 2005 Jun 29;25(26):6057-65
references.pmid: 15987935
references.citation: J Neurosci. 1997 May 15;17(10):3580-7
references.pmid: 9133381
references.citation: J Comp Neurol. 1988 Apr 1;270(1):11-24, 58-9
references.pmid: 3372732
references.citation: J Comp Neurol. 2004 Jan 12;468(3):311-21
references.pmid: 14681927
references.citation: J Neurosci. 2006 Feb 22;26(8):2227-34
references.pmid: 16495449
references.citation: J Comp Neurol. 2001 Nov 5;440(1):97-108
references.pmid: 11745610
references.citation: Ann N Y Acad Sci. 2002 Nov;976:356-66
references.pmid: 12502582
references.citation: J Neurophysiol. 2008 Mar;99(3):1503-14
references.pmid: 18199819
references.citation: Ann N Y Acad Sci. 1996 Apr 15;779:318-35
references.pmid: 8659845
references.citation: Trends Neurosci. 1988 Oct;11(10):438-43
references.pmid: 2469161
references.citation: Proc Natl Acad Sci U S A. 2007 Apr 10;104(15):6436-41
references.pmid: 17389364
references.citation: Prog Biophys Mol Biol. 2008 Jan-Apr;96(1-3):377-98
references.pmid: 17959231
references.citation: J Comp Neurol. 1985 May 1;235(1):48-60
references.pmid: 3989005
references.citation: J Comp Neurol. 1988 Apr 1;270(1):1-10, 56-7
references.pmid: 3372731
references.citation: J Neurosci. 1992 Dec;12(12):4898-904
references.pmid: 1464773
references.citation: J Biol Chem. 2002 Jan 4;277(1):1-4
references.pmid: 11696554
references.citation: J Neurosci. 2006 Apr 12;26(15):3971-80
references.pmid: 16611813
references.citation: Biophys J. 1977 Oct;20(1):79-111
references.pmid: 901903
references.citation: J Neurosci. 2003 Apr 1;23(7):2608-17
references.pmid: 12684446
references.citation: Cell. 2003 Feb 7;112(3):293-301
references.pmid: 12581520
references.citation: Crit Rev Eukaryot Gene Expr. 2008;18(2):125-37
references.pmid: 18304027
references.citation: J Neurosci. 2007 Oct 3;27(40):10840-8
references.pmid: 17913917
references.citation: Science. 2005 Dec 2;310(5753):1495-9
references.pmid: 16322458
references.citation: Science. 1988 Nov 18;242(4881):1047-50
references.pmid: 3194756
references.citation: J Comp Neurol. 2000 Aug 21;424(2):205-15
references.pmid: 10906698
references.citation: J Neurophysiol. 2008 Oct;100(4):2177-91
references.pmid: 18684902
references.citation: J Physiol. 2009 Aug 15;587(Pt 16):4077-89
references.pmid: 19581381
references.citation: Neuron. 1994 Nov;13(5):1109-17
references.pmid: 7524563
references.citation: Neuron. 1995 Nov;15(5):1077-84
references.pmid: 7576651
references.citation: Pflugers Arch. 2007 Aug;454(5):759-76
references.pmid: 17468883
references.citation: Nature. 2001 Sep 13;413(6852):219-25
references.pmid: 11557991
references.citation: Physiol Rev. 1999 Jul;79(3):763-854
references.pmid: 10390518
references.citation: J Physiol. 2003 Mar 1;547(Pt 2):475-83
references.pmid: 12562903
references.citation: Curr Biol. 2002 Aug 20;12(16):R563-5
references.pmid: 12194839