Tastants evoke a cAMP signal in taste buds that is independent of calcium signaling

We previously showed that rat taste buds express several adenylyl cyclases (ACs) of which, only AC8 is known to be stimulated by Ca 2+. Here, we demonstrate by direct measurements of cAMP levels, that AC activity in taste buds is stimulated by treatments that elevate intracellular Ca 2+. Specifically, 5 :M thapsigargin or 3 :M A23187 (calcium ionophore), both of which increase [Ca 2+ ] i , lead to a significant elevation of cAMP levels. This calcium-stimulation of AC activity requires extracellular Ca 2+ , suggesting that it is dependent on Ca 2+ entry, rather than release from stores. Using immunofluorescence microscopy, we show that the calcium-stimulated AC8 is principally expressed in taste cells that also express PLC$2 (i.e. cells that elevate [Ca 2+ ] i in response to sweet, bitter or umami 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 Ca 2+ may represent independent second messenger signals downstream of taste receptors.