The upper respiratory tract is continually assaulted with harmful dusts and xenobiotics carried on the incoming airstream. Detection of such irritants by the trigeminal nerve evokes protective reflexes, including sneezing, apnea, and local neurogenic inflammation of the mucosa. Although free intra-epithelial nerve endings can detect certain lipophilic irritants (e.g., mints, ammonia), the epithelium also houses a population of trigeminally innervated solitary chemosensory cells (SCCs) that express T2R bitter taste receptors along with their downstream signaling components. These SCCs have been postulated to enhance the chemoresponsive capabilities of the trigeminal irritant-detection system. Here we show that transduction by the intranasal solitary chemosensory cells is necessary to evoke trigeminally mediated reflex reactions to some irritants including acyl–homoserine lactone bacterial quorum-sensing molecules, which activate the downstream signaling effectors associated with bitter taste transduction. Isolated nasal chemosensory cells respond to the classic bitter ligand denatonium as well as to the bacterial signals by increasing intracellular Ca 2 + . Furthermore, these same substances evoke changes in respiration indicative of trigeminal activation. Genetic ablation of either Gα-gustducin or TrpM5, essential elements of the T2R transduction cascade, eliminates the trigeminal response. Because acyl–homoserine lactones serve as quorum-sensing molecules for Gram-negative pathogenic bacteria, detection of these substances by airway chemoreceptors offers a means by which the airway epithelium may trigger an epithelial inflammatory response before the bacteria reach population densities capable of forming destructive biofilms.
Rat taste buds contain three morphologically distinct cell types that are candidates for taste transduction. The physiologic roles of these cells are, however, not clear. Inositol 1,4,5-triphosphate (IP(3)) has been implicated as an important second messenger in bitter, sweet, and umami taste transductions. Previously, we identified the type III IP(3) receptor (IP(3)R3) as the dominant isoform in taste receptor cells. In addition, a recent study showed that phospholipase Cbeta(2) (PLCbeta(2)) is essential for the transduction of bitter, sweet, and umami stimuli. IP(3)R3 and PLCbeta(2) are expressed in the same subset of cells. To identify the taste cell types that express proteins involved in PLC signal transduction, we used 3,3'diaminobenzidine tetrahydrochloride immunoelectron microscopy and fluorescence microscopy to identify cells with IP(3)R3. Confocal microscopy was used to compare IP(3)R3 or PLCbeta(2) immunoreactivity with that of some known cell type markers such as serotonin, protein gene-regulated product 9.5, and neural cell adhesion molecule. Here we show that a large subset of type II cells and a small subset of type III cells display IP(3)R3 immunoreactivity within their cytoplasm. These data suggest that type II cells are the principal transducers of bitter, sweet, and umami taste transduction. However, we did not observe synapses between type II taste cells and nerve fibers. Interestingly, we observed subsurface cisternae of smooth endoplasmic reticulum at the close appositions between the plasma membrane of type II taste cells and nerve processes. We speculate that some type II cells may communicate to the nervous system via subsurface cisternae of smooth endoplasmic reticulum in lieu of conventional synapses.
Background: Taste receptor cells are responsible for transducing chemical stimuli from the environment and relaying information to the nervous system. Bitter, sweet and umami stimuli utilize G-protein coupled receptors which activate the phospholipase C (PLC) signaling pathway in Type II taste cells. However, it is not known how these cells communicate with the nervous system. Previous studies have shown that the subset of taste cells that expresses the T2R bitter receptors lack voltage-gated Ca 2+ channels, which are normally required for synaptic transmission at conventional synapses. Here we use two lines of transgenic mice expressing green fluorescent protein (GFP) from two taste-specific promoters to examine Ca 2+ signaling in subsets of Type II cells: T1R3-GFP mice were used to identify sweet-and umami-sensitive taste cells, while TRPM5-GFP mice were used to identify all cells that utilize the PLC signaling pathway for transduction. Voltage-gated Ca 2+ currents were assessed with Ca 2+ imaging and whole cell recording, while immunocytochemistry was used to detect expression of SNAP-25, a presynaptic SNARE protein that is associated with conventional synapses in taste cells.
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