Receptor and transduction processes for umami taste

The unique taste of umami argues for a specific receptor at the taste cell level. The taste synergism between monosodium glutamate (MSG) and certain 5 '-ribonucleotides provides a pharmacologic test for hypothetical mechanisms of umami taste. Early neurophysiologic and biochemical studies demonstrate d specific recognition of L-glutamate by taste tissue and suggested that th e synergism found with certain 5'-ribonucleotides was due to a peripheral e vent. The search fdr a receptor for umami relies at present on the data in the literature on central nervous system (CNS) glutamate receptors. These d ata distinguish several classes of receptors on the bases of pharmacologic properties and mode of action. Two hypotheses now seek to explain umami tas te transduction. One states that umami is transduced by an N-methyl-D-aspar tate (NMDA)-type glutamate ion channel receptor, the other that this taste is transduced via a metabotropic-type glutamate receptor. Evidence for the first hypothesis derives from earlier reconstitution studies, revealing a g lutamate-stimulated ion channel conductance whose kinetics were affected by 5'-ribonucleotides. Additional evidence is provided from more recent calci um-imaging and patch-clamp studies, both showing that an ionotropic-type re ceptor on rodent taste cells mediates glutamate-induced depolarization. Evi dence for the second mechanism derives from studies that located the messag e for an metabotropic-type (mGluR4) receptor to rat taste buds, and from wh ole-cell patch-clamp recordings that revealed sustained cellular conductanc es to glutamate and an mGluR4 agonist. It appears likely that both mechanis ms are involved in umami taste transduction, suggesting the possibility tha t reception and transduction of the umami signal constitute a collective pr operty of a number of cells within the taste bud.