Reception and transduction of glutamate signal in the taste bud

Abstract

Taste responses to glutamate are initiated by G-protein coupled receptors and transduced via G-protein signaling cascade, which ultimately activates the taste-transduction channel (TRPM5). Molecular genetics and heterologous expression implicate T1r1/T1r3 heterodimer as umami taste receptor. T1r3-KO mice, however, showed diminished but not abolished taste responses to glutamate, suggesting the existence of umami taste receptors other than T1r1/T1r3. Recordings from mouse single fibers and taste cells revealed that both glutamate sensitive fibers and taste cells were classified into sucrose-best (S-type) and mono potassium glutamate (MPG)-best (M-type). Each type was further classified into 2 subgroups: one type showing synergistic effect between MPG and IMP (S1, M1) and the other type showing no synergism (S2, M2). In T1R3- or TRPM5-KO mice, S1-type was absent, but S2, M1 and M2 types still remained, supporting the existence of multiple receptors, transduction pathways and fiber types for umami taste. Metabotropic glutamate receptors are possible umami taste receptors other than T1r1/T1r3. Group I and III antagonists, AIDA and CPPG, showed inhibitory effects on taste responses to glutamate, suggesting that mGluR1 and mGluR4 may be involved in glutamate signaling. Thus, taste of glutamate is mediated by multiple receptors and transduction mechanisms in the taste bud. [J Physiol Sci. 2008;58 Suppl:S27]