Abstract
TRPM5, a member of the transient receptor potential channel(TRP), is related with taste cell responses to sweet,umami and bitter compounds. Activation of TRPM5 occurs downstream activation of G-protein-coupled taste receptors and is proposed to generate a depolarizing potential in taste receptor cells. Mice with a partial deletion of the TRPM5 protein, which retained intact the amino terminal portion, have been shown to be unresponsive to bitter, sweet, umami tastes. To avoid any confounding effects of this amino terminal fragment, we generated knockout mice null for TRPM5 protein. In previous study, this TRPM5 knockout mice showed reduced, but not abolished, responses to quinine hydrochloride in both nerve recording and two-bottle preference test. In this study, in order to examine behavioral responses to quinine hydrochloride in TRPM5 knockout mice in further detail, we used a short-term (10s) lick test for measurement of consumption of its solutions. TRPM5 knockout mice showed significantly reduced responses to 0.1-10 mM quinine hydrochloride, but not abolished at high concentrations (3.0,10mM) of it, although no such difference was evident in response to DW. These results may be almost consistent with previous nerve recording and two-bottle preference test, suggesting that there may be TRPM5-dependent and independent pathways in signal transduction mechanism for quinine hydrochloride.. [J Physiol Sci. 2006;56 Suppl:S184]
