Genetic Tracing of the Gustatory Neural Pathway Originating from T1R3-expressing Sweet/Umami Taste Receptor Cells

2009 ◽  
Vol 1170 (1) ◽  
pp. 46-50 ◽  
Author(s):  
Ichiro Matsumoto ◽  
Makoto Ohmoto ◽  
Akihito Yasuoka ◽  
Yoshihiro Yoshihara ◽  
Keiko Abe
Keyword(s):  
Taste Receptor ◽  
Neural Pathway ◽  
Umami Taste ◽  
Receptor Cells ◽  
Taste Receptor Cells

scholarly journals Taste Receptor Cells in Mice Express Receptors for the Hormone Adiponectin

2018 ◽  
Author(s):  
Sean M. Crosson ◽  
Andrew Marques ◽  
Peter Dib ◽  
Cedrick D. Dotson ◽  
Steven D. Munger ◽  
...  
Keyword(s):  
Cell Function ◽  
Receptor Cell ◽  
Taste Receptor ◽  
Acid Oxidation ◽  
Taste Receptor Cell ◽  
Umami Taste ◽  
Receptor Cells ◽  
Taste Receptor Cells ◽  
Immunohistochemical Studies ◽  
Adipocyte Development

AbstractThe metabolic hormone adiponectin is secreted into the circulation by adipocytes, and mediates key biological functions including insulin sensitivity, adipocyte development, and fatty acid oxidation. Adiponectin is also abundant in saliva, where its functions are poorly understood. Here we report that murine taste receptor cells express adiponectin receptors, and may be a target for salivary adiponectin. Analysis of a transcriptome dataset obtained by RNA-seq analysis of purified circumvallate taste buds, revealed high expression levels for three adiponectin receptor types. Immunohistochemical studies showed that two of these receptors, AdipoR1 and T-cadherin, are localized to subsets of taste receptor cells. Immunofluorescence for T-cadherin was primarily co-localized with the Type 2 taste receptor cell marker phospholipase β2, suggesting that adiponectin signaling could impact sweet, bitter, or umami taste signaling. However, adiponectin null mice showed no differences in taste responsiveness compared to wildtype controls in brief-access taste testing. AAV-mediated overexpression of adiponectin in the salivary glands of adiponectin null mice did result in a small but significant increase in behavioral taste responsiveness to the fat emulsion Intralipid. Together, these results suggest that salivary adiponectin can effect taste receptor cell function, though its impact on taste responsiveness and peripheral taste coding remains unclear.

scholarly journals Responses to Di-Sodium Guanosine 5′-Monophosphate and Monosodiuml-Glutamate in Taste Receptor Cells of Rat Fungiform Papillae

2003 ◽  
Vol 89 (3) ◽  
pp. 1434-1439 ◽  
Author(s):  
Weihong Lin ◽  
Tatsuya Ogura ◽  
Sue C. Kinnamon
Keyword(s):  
Patch Clamp ◽  
Monosodium Glutamate ◽  
Taste Receptor ◽  
Intracellular Camp ◽  
Fungiform Papillae ◽  
Simultaneous Application ◽  
Umami Taste ◽  
Receptor Cells ◽  
Imaging Results ◽  
Taste Receptor Cells

The 5′-ribonucleotide guanosine 5′-monophosphate (GMP) is used widely as an umami taste stimulus and a potent flavor enhancer as it synergistically increases the umami taste elicited by monosodium glutamate. Transduction mechanisms for GMP and its synergy with glutamate are largely unknown. Using whole-cell patch-clamp and Ca2+ imaging, we examined responses to GMP, glutamate, and a mixture of GMP and glutamate in taste-receptor cells of rat fungiform papillae. Our electrophysiological results showed that GMP induces responses that are similar to those of glutamate, e.g., an outward current, an inward current, or a biphasic response. Our Ca2+ imaging results showed that applications of GMP, glutamate, and the mixture increased intracellular Ca2+ levels. Interestingly, both patch-clamp and Ca2+ imaging showed that some taste cells can respond to GMP and glutamate independently, indicating that glutamate and GMP likely activate different receptors. Simultaneous application of GMP and glutamate resulted in synergistic responses in a subset of cells; both response intensity and number of responding cells were increased. Most responses to GMP, as well as the synergy between GMP and glutamate, were suppressed by 8bromo-adenosine 3′,5′-cyclic monophosphate (8-bromo-cAMP) in patch-clamp recordings. Together, our results suggest that intracellular cAMP- and Ca2+-mediated pathways are involved in umami taste transduction for GMP and its synergistic responses with glutamate.

scholarly journals Taste Receptor Cells in Mice Express Receptors for the Hormone Adiponectin

2019 ◽  
Vol 44 (6) ◽  
pp. 409-422 ◽  
Author(s):  
Sean M Crosson ◽  
Andrew Marques ◽  
Peter Dib ◽  
Cedrick D Dotson ◽  
Steven D Munger ◽  
...  
Keyword(s):  
Taste Receptor ◽  
Immunohistochemical Analysis ◽  
Acid Oxidation ◽  
Rna Seq ◽  
Adiponectin Receptors ◽  
Umami Taste ◽  
Receptor Cells ◽  
Taste Receptor Cells ◽  
Adipocyte Development

Abstract The metabolic hormone adiponectin is secreted into the circulation by adipocytes and mediates key biological functions, including insulin sensitivity, adipocyte development, and fatty acid oxidation. Adiponectin is also abundant in saliva, where its functions are poorly understood. Here we report that murine taste receptor cells (TRCs) express specific adiponectin receptors and may be a target for salivary adiponectin. This is supported by the presence of all three known adiponectin receptors in transcriptomic data obtained by RNA-seq analysis of purified circumvallate (CV) taste buds. As well, immunohistochemical analysis of murine CV papillae showed that two adiponectin receptors, ADIPOR1 and T-cadherin, are localized to subsets of TRCs. Immunofluorescence for T-cadherin was primarily co-localized with the Type 2 TRC marker phospholipase C β2, suggesting that adiponectin signaling could impact sweet, bitter, or umami taste signaling. However, adiponectin null mice showed no differences in behavioral lick responsiveness compared with wild-type controls in brief-access lick testing. AAV-mediated overexpression of adiponectin in the salivary glands of adiponectin null mice did result in a small but significant increase in behavioral lick responsiveness to the fat emulsion Intralipid. Together, these results suggest that salivary adiponectin can affect TRC function, although its impact on taste responsiveness and peripheral taste coding remains unclear.

Taste Transductions in Taste Receptor Cells: Basic Tastes and Moreover

2014 ◽  
Vol 20 (16) ◽  
pp. 2684-2692 ◽  
Author(s):  
Shusuke Iwata ◽  
Ryusuke Yoshida ◽  
Yuzo Ninomiya
Keyword(s):  
Taste Receptor ◽  
Receptor Cells ◽  
Taste Receptor Cells

scholarly journals Role for epithelial Na+channels and putative Na+/H+ exchangers in salt taste transduction in rats

1997 ◽  
Vol 273 (6) ◽  
pp. R1923-R1931 ◽  
Author(s):  
Robert F. Lundy ◽  
David W. Pittman ◽  
Robert J. Contreras
Keyword(s):  
Salt Concentration ◽  
Taste Receptor ◽  
Drug Dose ◽  
Chorda Tympani Nerve ◽  
Sprague Dawley ◽  
Salt Taste ◽  
Receptor Cells ◽  
Taste Transduction ◽  
Taste Receptor Cells ◽  
Dimethyl Amiloride

The effects of the epithelial Na+channel antagonists amiloride and benzamil and the Na+/H+exchange antagonist 5-( N, N-dimethyl)-amiloride (DMA)-Cl on the integrated responses of the chorda tympani nerve to 30, 75, 150, 300, and 500 mM concentrations of NaCl, KCl, and NH4Cl were assessed in male Sprague-Dawley rats. Based on evidence from other systems, 1 and 25 μM amiloride and benzamil were chosen to selectively inhibit epithelial Na+ channels and 1 μM DMA was chosen to selectively inhibit Na+/H+exchange. When added to stimulating salt solutions, amiloride, benzamil, and DMA were each effective in inhibiting responses to all three salts. The degree of inhibition varied with drug, salt, and salt concentration, but not drug dose. Amiloride suppressed NaCl responses to a greater degree than KCl and NH4Cl responses, whereas DMA suppressed NH4Cl responses to a greater degree than NaCl and KCl responses. In all but one case (25 μM amiloride added to KCl), drug suppression of taste nerve responses decreased with an increase in salt concentration. The present results suggest that 1) epithelial Na+ channels in rat taste receptor cells may play a role in KCl and NH4Cl taste transduction; 2) a Na+/H+exchange protein may be present in taste receptor cells, representing a putative component, in addition to epithelial Na+ channels, in salt taste transduction; and 3) salt taste detection and transduction may depend on the utilization of a combination of common and distinct transcellular pathways.

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