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Electrophysiological responses to sugars and amino acids in the nucleus of the solitary tract of type 1 taste receptor double knockout mice.

Strong evidence supports a major role for heterodimers of the Type 1 taste receptor (T1R) family in the taste transduction of sugars (T1R2+T1R3) and amino acids (T1R1+T1R3), but there are also neural and behavioral data supporting T1R-independent mechanisms. Most neural evidence for alternate mechanisms comes from whole-nerve recordings in mice with deletion of a single T1R family member, limiting conclusions about the functional significance and T1R independence of the remaining responses. To clarify these issues, we recorded single-unit taste responses from the nucleus of the solitary tract (NST) in T1R double-knockout (double-KO) mice lacking functional T1R1+T1R3 [KO1+3] or T1R2+T1R3 [KO2+3] receptors and their WT background strains (WT; (C57BL/6J [B6], 129X1/SvJ [S129]). In both double-KO strains, responses to sugars and a moderate concentration of an MSG+amiloride+IMP cocktail (0.1M, i.e, umami) were profoundly depressed, whereas a panel of 0.6M amino acids were mostly unaffected. Strikingly, in contrast to WT mice, no double-KO neurons responded selectively to sugars and umami, precluding segregation of this group of stimuli from those representing other taste qualities in a multidimensional scaling analysis. Nevertheless, residual sugar responses, mainly elicited by monosaccharides, persisted as small "sideband" responses in double-KO's. Thus, other receptors may convey limited information about sugars to the CNS but T1R's appear critical for coding the distinct perceptual features of sugar and umami stimuli. The persistence of amino acid responses supports previous proposals of alternate receptors, but because these stimuli affected multiple neuron types, further investigations are necessary.