| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Dept of Physiology and Biophysics, University of Miami Miller School of Medicine, Miami, FL, USA
2 Dept of Biomedical Sciences, Colorado State University, Ft. Collins, CO, USA
3 Dept of Physiology and Biophysics, University of Miami Miller School of Medicine, Miami, FL, USA; Neuroscience Program, University of Miami Miller School of Medicine, Miami, FL, USA
* To whom correspondence should be addressed. E-mail: nchaudhari{at}miami.edu.
We previously showed that rat taste buds express several adenylyl cyclases (ACs) of which, only AC8 is known to be stimulated by Ca2+. Here, we demonstrate by direct measurements of cAMP levels, that AC activity in taste buds is stimulated by treatments that elevate intracellular Ca2+. Specifically, 5 µM thapsigargin or 3 µM A23187(calcium ionophore), both of which cause a increase in [Ca2+]i lead to a significant elevation of cAMP levels. This calcium-stimulation of AC activity requires extracellular Ca2+, indicating that it is dependent on Ca2+ entry, rather than release from stores. Using immunofluorescence microscopy, we show that the calcium-stimulated AC8 is principally expressed in cells that also express PLC
2 (i.e. cells that elevate [Ca2+]i in response to sweet, bitter or umami taste stimuli). Taste transduction for sucrose is known to result in an elevation of both cAMP and calcium in taste buds. Thus, we tested whether the cAMP increase in response to sucrose is a downstream consequence of calcium elevation. Even under conditions of depletion of stored and extracellular calcium, the cAMP response to sucrose stimulation persists in taste cells. The cAMP signal in response to MSG stimulation is similarly unperturbed by calcium depletion. Our results suggest that tastant-evoked cAMP signals are not simply a secondary consequence of calcium modulation. Instead, cAMP and released Ca2+ may represent independent second messenger signals downstream of taste receptors.
This article has been cited by other articles:
|
|
 |
|
  N. Chaudhari, E. Pereira, and S. D Roper Taste receptors for umami: the case for multiple receptors Am. J. Clinical Nutrition, September 1, 2009; 90(3): 738S - 742S. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. D. Roberts, G. Dvoryanchikov, S. D. Roper, and N. Chaudhari Interaction between the second messengers cAMP and Ca2+ in mouse presynaptic taste cells J. Physiol., April 15, 2009; 587(8): 1657 - 1668. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Ohkuri, K. Yasumatsu, N. Horio, M. Jyotaki, R. F. Margolskee, and Y. Ninomiya Multiple sweet receptors and transduction pathways revealed in knockout mice by temperature dependence and gurmarin sensitivity Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2009; 296(4): R960 - R971. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. K. Palmer The Pharmacology and Signaling of Bitter, Sweet, and Umami Taste Sensing Mol. Interv., April 1, 2007; 7(2): 87 - 98. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
