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 demonstrated specific recognition of L-glutamate by taste tissue and suggested that the synergism found with certain 5'-ribonucleotides was due to a peripheral event. The search for a receptor for umami relies at present on the data in the literature on central nervous system (CNS) glutamate receptors. These data distinguish several classes of receptors on the bases of pharmacologic properties and mode of action. Two hypotheses now seek to explain umami taste transduction. One states that umami is transduced by an N-methyl-D-aspartate (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 glutamate-stimulated ion channel conductance whose kinetics were affected by 5'-ribonucleotides. Additional evidence is provided from more recent calcium-imaging and patch-clamp studies, both showing that an ionotropic-type receptor on rodent taste cells mediates glutamate-induced depolarization. Evidence for the second mechanism derives from studies that located the message for an metabotropic-type (mGluR4) receptor to rat taste buds, and from whole-cell patch-clamp recordings that revealed sustained cellular conductances to glutamate and an mGluR4 agonist. It appears likely that both mechanisms are involved in umami taste transduction, suggesting the possibility that reception and transduction of the umami signal constitute a collective property of a number of cells within the taste bud.