Lu Shao-gang, Zhao Fang-li, Herness Scott
Section of Oral Biology, College of Dentistry, The Ohio State University, 305 West 12th Avenue, Columbus, OH 43210, USA.
Neurosci Lett. 2003 Nov 20;351(3):157-60. doi: 10.1016/j.neulet.2003.07.016.
The recent discovery that subsets of rat taste receptor cells (TRCs) express the peptide cholecystokinin (CCK) and that subsets of TRCs respond to CCK with altered potassium currents or elevated intracellular calcium via CCK-A receptor has lead to the hypothesis that CCK may play a novel signaling role within the taste bud, perhaps modifying tastant responses by co-transmission with a classic transmitter. To better understand this phenomenon, CCK-responsive TRCs were characterized for sensitivity to two bitter stimuli, quinine or caffeine, or to the neurotransmitter ACh using a ratiometric procedure with the calcium sensitive dye fura-2. In characterizing TRC responses to quinine, it was observed that quinine-induced elevations of intracellular calcium were not due to endogenous fluorescence of the quinine molecule. Most (60-70%) CCK-responsive cells were also sensitive to either bitter stimuli or to cholinergic stimulation. These data suggest that TRCs expressing CCK-receptors also express receptors to bitter stimuli and/or muscarinic receptors. They further support the notion of a putative modulatory role of CCK with convergence of multiple inputs occurring at the level of intracellular calcium.