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1 Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California, United States
* To whom correspondence should be addressed. E-mail: erozengurt{at}mednet.ucla.edu.
We previously demonstrated the expression of bitter taste receptors of the type 2 family (T2R) and the 
subunits of the G protein gustducin (Ggust) in the rodent gastrointestinal (GI) tract and in GI endocrine cells. Here, we characterized mechanisms of Ca2+ fluxes induced by two distinct T2R ligands: denatonium benzoate (DB) and phenylthiocarbamide (PTC), in mouse enteroendocrine cell line STC-1. Both DB and PTC induced a marked increase in intracellular Ca2+ concentration ([Ca2+]i) in a dose- and time-dependent maner. Chelating extracellular Ca2+ with EGTA blocked the increase in [Ca2+]i induced by either DB or PTC but, in contrast, did not prevent the effect induced by bombesin. Thapsigargin blocked the transient increase in [Ca2+]i induced by bombesin, but did not attenuate the [Ca2+]i increase elicited by DB or PTC. These results indicate that Ca2+ influx mediates the increase in [Ca2+]i induced by DB and PTC in STC-1 cells. Preincubation with the L-type voltage-sensitive Ca2+ channel (L-type VSCCs) blockers nitrendipine or diltiazem for 30 min inhibited the increase in [Ca2+]i elicited by DB or PTC. Furthermore, exposure to the L-type VSCCs opener Bay-K8644 potentiated the increase in [Ca2+]i induced by DB and PTC. Stimulation with DB also induced a marked increase in the release of cholecystokinin (CCK) from STC-1 cells, an effect also abrogated by prior exposure to EGTA or L-type VSCCs blockers. Collectively, our results demonstrate that bitter tastants increase [Ca2+]i and CCK release through Ca2+ influx mediated by the opening of L-type VSCCs in enteroendocrine STC-1 cells.
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