Diverse contributions of Tas1r2/Tas2rs within the rat and mouse soft palate to sweet and bitter neural responses.

Neural responses to sweet and bitter stimuli in the rat and mouse are compared to the expression of the molecular taste receptors, Tas1r2/Tas2rs. Integrated taste responses from the greater superficial petrosal nerve (GSP) innervating the soft palate (SP) and the chorda tympani (CT) nerve innervating the fungiform papillae (FF) were recorded in C57BL mice and SD rats. The sum of the phasic and tonic response magnitudes (SRM) was calculated by summating all relative mean responses to a concentration series of QHCl (10(-6)-10(-2)M) or Suc (10(-4)-1.0M). Molecular expression was analyzed by double-colored in situ hybridization for Gα-gustducin with Tas1r2 or Tas2rs in the SP and FF. The vast majority of cells expressing Tas1r2 or Tas2rs were included in Gα-gustducin-expressing cells in the SP of both species. Unexpectedly, a comparison between species revealed that the SRM from the GSP is not positively correlated with receptor expression in the SP. In the rat SP, the percentage of Tas2rs with Gα-gustducin (Tas2rs/gust, 65%) was twice larger than that for Tas1r2/gust (33%), while the SRM to Suc in the rat GSP was 1.5 times (tonic and phasic) larger than that to QHCl. In the mouse SP, the percentage of Tas2rs/gust (46%) was less than that in the rat and similar to that of Tas1r2/gust (40%). However, the SRM to QHCl in the mouse GSP was 2.4 (phasic) and 4.7 (tonic) times larger than to Suc. On the other hand, threshold to Suc in the rat GSP was 10(-3)M, one log unit lower than in mouse, and the threshold to QHCl in the mouse GSP was 10(-6)M, one log unit lower than in rat. These results suggest that the robust GSP response to Suc in rat and to QHCl in mouse likely do not depend upon a large number of taste cells expressing the taste receptors Tas1r2 for Suc or Tas2rs for QHCl, but upon a higher density of Tas1r2/Tas2rs within the respective taste cells of the two species.

Tomonari H ，Miura H ，Ooki M ，Nakayama A ，Harada S ... -  《-》

Gα-gustducin is extensively coexpressed with sweet and bitter taste receptors in both the soft palate and fungiform papillae but has a different functional significance.

Tomonari H ，Miura H ，Nakayama A ，Matsumura E ，Ooki M ，Ninomiya Y ，Harada S ... -  《-》

Expression of gustducin overlaps with that of type III IP3 receptor in taste buds of the rat soft palate.

Miura H ，Nakayama A ，Shindo Y ，Kusakabe Y ，Tomonari H ，Harada S ... -  《CHEMICAL SENSES》

Different characteristics of gustatory responses between the greater superficial petrosal and chorda tympani nerves in the rat.

Harada S ，Yamamoto T ，Yamaguchi K ，Kasahara Y ... -  《CHEMICAL SENSES》

Ingestion of bacterial lipopolysaccharide inhibits peripheral taste responses to sucrose in mice.

A fundamental role of the taste system is to discriminate between nutritive and toxic foods. However, it is unknown whether bacterial pathogens that might contaminate food and water modulate the transmission of taste input to the brain. We hypothesized that exogenous, bacterially-derived lipopolysaccharide (LPS), modulates neural responses to taste stimuli. Neurophysiological responses from the chorda tympani nerve, which innervates taste cells on the anterior tongue, were unchanged by acute exposure to LPS. Instead, neural responses to sucrose were selectively inhibited in mice that drank LPS during a single overnight period. Decreased sucrose sensitivity appeared 7days after LPS ingestion, in parallel with decreased lingual expression of Tas1r2 and Tas1r3 transcripts, which are translated to T1R2+T1R3 subunits forming the sweet taste receptor. Tas1r2 and Tas1r3 mRNA expression levels and neural responses to sucrose were restored by 14 days after LPS consumption. Ingestion of LPS, rather than contact with taste receptor cells, appears to be necessary to suppress sucrose responses. Furthermore, mice lacking the Toll-like receptor (TLR) 4 for LPS were resistant to neurophysiological changes following LPS consumption. These findings demonstrate that ingestion of LPS during a single period specifically and transiently inhibits neural responses to sucrose. We suggest that LPS drinking initiates TLR4-dependent hormonal signals that downregulate sweet taste receptor genes in taste buds. Delayed inhibition of sweet taste signaling may influence food selection and the complex interplay between gastrointestinal bacteria and obesity.

Zhu X ，He L ，McCluskey LP 《-》