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Glutamate transduction mechanism in mouse taste cells

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image of Sensory Neuron
For more content, see Primary Sensory Neuron.

In order to clarify the role of group III metabotropic glutamate receptor (including mGluR4) in transduction for umami taste, we investigated the effects of monosodium glutamate (MSG) and 2-amino-4-phosphonobutyrate (L-AP4), a mGluR4 agonist, on taste cells by use of electrophysiological and biochemical methods, and Ca2+ imaging in C57BL mice. The responses of the chorda tympani (CT) nerve to MSG were suppressed by gurmarin, a sweet response inhibitor, indicating that the MSG response may be partly mediated by sweet receptors, while the CT responses to L-AP4 and the glossopharyngeal (GL) nerve responses to MSG were little suppressed by gurmarin suggesting that these responses may be mediated by only umami receptors. Biochemical study demonstrated that MSG stimulation significantly elevated both adenosine 3′, 5′-cyclic monophosphate (cAMP) and inositol 1,4,5-triphosphate (IP3) levels in the fungiform papillae. The increase in cAMP might occur through sweet receptors, which is consistent with CT nerve responses. The increase in IP3 levels may relate to intracellular events mediated by group III mGluRs, because MSG and L-AP4 induced increment of intracellular Ca2+ concentration in some taste cells. Whole-cell patchclamp recording from isolated taste cells showed that L-AP4 induced not only outward currents with a conductance decreases but also inward currents with conductance increases at about resting potentials. These inward currents reversed at +10-+30 mV suggesting that cation conductance was activated by L-AP4. These results strongly support the idea that phospholipase C activation mediated by group III mGluRs is involved in transduction mechanism for umami taste, and also suggest the possibility that stimulation of the mGluRs may cause activation of cation conductance as well as [Ca2+]i elevation.


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