Humans have five established basic tastes: sweet, sour, bitter, salt, and umami. The umami taste was added to the four classic tastes relatively recently, but it has been known for almost 100 years. It became established as a taste modality once its receptor was identified. It is triggered particularly by the monosodium glutamate (MSG) used so extensively in Asian cooking. The taste is pleasant and sweet but differs from the standard sweet taste. Although for many years it was thought that the surface of the tongue had special areas for each of the first four of these sensations, it is now known that all tastants are sensed from all parts of the tongue and adjacent structures. Afferent nerves to the NTS contain fibers from all types of taste receptors, without any clear localization of types.
The putative receptors for the five modalities of taste are shown diagrammatically in Figure 1. They include the two major types of receptors: ligand-gated channels (ionotropic receptors) and GPCRs (metabotropic receptors). Salt and sour tastes are triggered by activation of ionotropic receptors; sour, bitter, and umami tastes are triggered by activation of metabotropic receptors. Many GPCRs in the human genome are taste receptors type (T1R1, T1R2, and T1R3 families). In some cases, these receptors couple to the heterotrimeric G-protein, gustducin. Gustducin lowers cAMP and increases the formation of inositol phosphates (IP3 ), which can lead to depolarization.
Fig1. Signal transduction in taste receptors. Salt and sour tastes are mediated via the epithelial sodium channel (ENaC). This receptor has two subunits (α and γ), each crossing the membrane twice, resulting in intracellular N and C termini (NT, CT). Salt is sensed following Na+ movement; sour is mediated by movement of H+. Sweet, bitter, and umami tastes are sensed via G-protein–coupled receptors that span the membrane seven times and have varying lengths of CT and NT (represented as ribbon structures). Sweet tastes are detected by the T1R2 and T1R3 families; bitter and umami tastes are detected by the T2R family and mGluR4, respectively.
The salty taste is triggered by NaCl. Salt-sensitive taste is mediated by an epithelial sodium channel (ENaC). The entry of Na+ into the salt receptors depolarizes the mem brane, generating the receptor potential. The sour taste is triggered by protons (H+ ions). ENaCs permit the entry of protons and may contribute to the sensation of sour taste. The H+ ions can also bind to and block a K+-sensitive channel. The fall in K+ permeability can depolarize the membrane. Also, a hyperpolarization-activated cyclic nucleotide-gated cation channel (HCN) and other mechanisms may contribute to sour transduction.
Substances that taste sweet are detected by at least two types of GPCRs, T1R2 and T1R3. Sugars taste sweet, but so do compounds such as saccharin that have an entirely different structure. Natural sugars such as sucrose and synthetic sweeteners may act on gustducin via different receptors. Sweet responsive receptors act via cyclic nucleotides and inositol phosphate metabolism.
Bitter taste is produced by a variety of unrelated com pounds. Many of these are poisons, and bitter taste serves as a warning to avoid them. Some bitter compounds bind to and block K+-selective channels. Many GPCRs (T2R family) that interact with gustducin are stimulated by bitter substances such as strychnine. Some bitter compounds are membrane permeable and their detection may not involve G-proteins; quinine is an example.
Umami taste is due to the activation of a truncated metabotropic glutamate receptor, mGluR4, in the taste buds. The way activation of the receptor produces depolarization is unsettled. Glutamate in food may also activate ionotropic glutamate receptors to depolarize umami receptors. It is likely that T1R1 and T1R3 receptors also detect umami taste.
