Physiological evidence for ionotropic and metabotropic glutamate receptorsin rat taste cells

Monosodium glutamate (MSG) elicits a unique taste in humans called umami. R ecent molecular studies suggest that glutamate receptors similar to those i n brain are present in taste cells, but their precise role in taste transdu ction remains to be elucidated. We used giga-seal whole cell recording to e xamine the effects of MSG and glutamate receptor agonists on membrane prope rties of taste cells from rat fungiform papillae. MSG (1 mM) induced three subsets of responses in cells voltage-clamped at -80 mV: a decrease in hold ing current (subset I), an increase in holding current (subset II), and a b iphasic response consisting of an increase, followed by a decrease in holdi ng current (subset III). Most subset II glutamate responses were mimicked b y the ionotropic glutamate receptor (iGluR) agonist N-methyl-D-aspartate (N MDA). The current was potentiated by glycine and was suppressed by the NMDA receptor antagonist D(-)-2-amino-5-phosphonopentanoic acid (AP5). The grou p III metabotropic glutamate receptor (mGluR) agonist L-2-amino-4-phosphono butyric acid (L-Ap4) usually mimicked the subset I glutamate response. This hyperpolarizing response was suppressed by the mGluR antagonist (RS)-alpha -cyclopropyl-4-phosphonophenyl-glycine (CPPG) and by 8-bromo-cAMP, suggesti ng a role for cAMP in the transduction pathway. In a small subset of taste cells, L-AP4 elicited an increase in holding current, resulting in taste ce ll depolarization under current clamp. Taken together, our results suggest that NMDA-like receptors and at least two types of group III mGluRs are pre sent in taste receptor cells, and these may be coactivated by MSG. Further studies are required to determine which receptors are located on the apical membrane and how they contribute to the umami taste.