Rapid kinetics of second messenger production in bitter taste

Abstract

The tasting of bitter compounds may have evolved as a protective mechanism against ingestion of potentially harmful substances. We have identified second messengers involved in bitter taste and show here for the first time that they are rapid and transient. Using a quench-flow system, we have studied bitter taste signal transduction in a pair of mouse strains that differ in their ability to taste the bitter stimulus sucrose octaacetate (SOA); however, both strains taste the bitter agent denatonium. In both strains of mice, denatonium (10 mM) induced a transient and rapid increase in levels of the second messenger inositol 1,4,5-trisphosphate (IP3) with a maximal production near 75-100 ms after stimulation. In contrast, SOA (100 microM) brought about a similar increase in IP3 only in SOA-taster mice. The response to SOA was potentiated in the presence of GTP (1 microM). The GTP-enhanced SOA-response supports a G protein-mediated response for this bitter compound. The rapid kinetics, transient nature, and specificity of the bitter taste stimulus-induced IP3 formation are consistent with the role of IP3 as a second messenger in the chemoelectrical transduction of bitter taste.

Mouse Taste Buds Use Serotonin as a Neurotransmitter

“…taste cells via a signaling cascade involving phospholipase C ␤2 (PLC␤2) and IP 3 (Bernhardt et al, 1996;Spielman et al, 1996). Thus, a likely source of Ca 2ϩ for transmitter release elicited by these compounds was an intracellular store.…”

Signal transduction and information processing in mammalian taste buds

“…The proteins and other mediators involved in this second messenger cascade have been identified in taste cells, including the discovery of a taste-specific isoform of phospholipase C (PLCβ2) [112], the presence of IP3R3 receptors in taste cells [113], the measurement of taste-evoked IP3 increases [114,115], and the all-important observation that taste stimulation indeed evokes intracellular Ca 2+ release [116,117]. Notably, single-cell PCR experiments show that all the proteins in the PLCβ2-IP3-Ca 2+ pathway are expressed in the same cell, the taste receptor cell [118,119].…”

Separate Populations of Receptor Cells and Presynaptic Cells in Mouse Taste Buds

“…Knock-out of the PlCb2 gene leads to profound taste deficits (Zhang et al, 2003;Dotson et al, 2005). These and other findings indicate that chemosensory transduction for bitter, sweet, and umami is predominantly mediated through a shared signaling pathway that involves phosphoinositide-mediated release of stored intracellular Ca 2ϩ (Akabas et al, 1988;Spielman et al, 1996;Caicedo and Roper, 2001).…”