P-29. Neurobiology and taste transduction mechanisms of taste buds

Kuniaki Toyoshima; Yuji Seta; Takashi Toyono; Shinji Kataoka

doi:10.2504/kds.58.147_2

Taste

Sensory Transduction ◽

10.1093/oso/9780198835028.003.0008 ◽

2019 ◽

pp. 159-177

Author(s):

Gordon L. Fain

Keyword(s):

Neural Code ◽

Taste Buds ◽

Sensory Transduction ◽

Receptor Proteins ◽

Taste Transduction ◽

Signal Production

“Taste” is the eighth chapter of the book Sensory Transduction and begins with gustation in insects, describing receptor proteins in insect taste organs and mechanisms of signal production. It proceeds to the anatomy of taste buds and the tongue in mammals and describes the two basic forms of taste transduction: metabotropic and ionotropic. For metabotropic mechanisms, a thorough review is given of the receptor proteins and signal production for bitter, sweet, and umami, concluding with common pathways of transduction for these modalities. The separate ionotropic mechanisms of salty and sour are then reviewed, and the chapter concludes with discussion of our understanding of the neural code for taste.

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Self-Inhibition in Ca2+-Evoked Taste Responses: A Novel Tool for Functional Dissection of Salt Taste Transduction Mechanisms

Journal of Neurophysiology ◽

10.1152/jn.1998.79.2.911 ◽

1998 ◽

Vol 79 (2) ◽

pp. 911-921 ◽

Cited By ~ 7

Author(s):

Mamoun A. Kloub ◽

Gerard L. Heck ◽

John A. Desimone

Keyword(s):

Tight Junctions ◽

Ion Selectivity ◽

Critical Concentration ◽

Dependent Manner ◽

High Concentration ◽

Salt Taste ◽

Cation Conductance ◽

Taste Transduction ◽

Transduction Mechanisms ◽

Paracellular Pathways

Kloub, Mamoun A., Gerard L. Heck, and John A. DeSimone. Self-inhibition in Ca2+-evoked taste receptors: a novel tool for functional dissection of salt taste transduction mechanisms. J. Neurophysiol. 79: 911–921, 1998. Rat chorda tympani (CT) responses to CaCl2 were obtained during simultaneous current and voltage clamping of the lingual receptive field. Unlike most other salts, CaCl2 induced negatively directed transepithelial potentials and gave CT responses that were auto-inhibitory beyond a critical concentration. CT responses increased in a dose-dependent manner to ∼0.3 M, whereafter they decreased with increasing concentration. At concentrations where Ca2+ was self-inhibitory, it also inhibited responses to NaCl, KCl, and NH4Cl present in mixtures with CaCl2. Ca2+ completely blocked the amiloride-insensitive component of the NaCl CT response, the entire KCl-evoked CT response, and the high-concentration-domain CT responses of NH4Cl (≥0.3 M). The overlapping Ca2+-sensitivity between the responses of the three Cl− salts (Na+, K+, and NH+ 4) suggests a common, Ca2+-sensitive, transduction pathway. Extracellular Ca2+ has been shown to modulate the paracellular pathways in different epithelial cell lines by decreasing the water permeability and cation conductance of tight junctions. Ca2+-induced modulation of tight junctions is associated with Ca2+ binding to fixed negative sites. This results in a conversion of ion selectivity from cationic to anionic, which we also observed in our system through simultaneous monitoring of the transepithelial potential during CT recording. The data indicate the paracellular pathway as the stimulatory and modulatory site of CaCl2 taste responses. In addition, they indicate that important transduction sites for NaCl, KCl, and NH4Cl taste reception are accessible only through the paracellular pathways. More generally, they show that modulation of paracellular transport by Ca2+ in an intact epithelium has functional consequences at a systemic level.

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Sweet Taste Transduction in Hamster: Role of Protein Kinases

Journal of Neurophysiology ◽

10.1152/jn.2000.83.5.2526 ◽

2000 ◽

Vol 83 (5) ◽

pp. 2526-2532 ◽

Cited By ~ 25

Author(s):

Brian Varkevisser ◽

Sue C. Kinnamon

Keyword(s):

Protein Kinase ◽

Protein Kinases ◽

Sweet Taste ◽

Taste Buds ◽

Regulatory Proteins ◽

Camp Phosphodiesterase ◽

Kinase C ◽

Taste Transduction ◽

Second Messenger Pathways

Two different second-messenger pathways have been implicated in sweet taste transduction: sugars produce cyclic AMP (cAMP), whereas synthetic sweeteners stimulate production of inositol 1,4,5-tris-phosphate (IP3) and diacylglycerol (DAG). Both sugars and sweeteners depolarize taste cells by blocking the same resting K+conductance, but the intermediate steps in the transduction pathways have not been examined. In this study, the loose-patch recording technique was used to examine the role of protein kinases and other downstream regulatory proteins in the two sweet transduction pathways. Bursts of action currents were elicited from ∼35% of fungiform taste buds in response to sucrose (200 mM) or NC-00274–01 (NC-01, 200 μM), a synthetic sweetener. To determine whether protein kinase C (PKC) plays a role in sweet transduction, taste buds were stimulated with the PKC activator PDBu (10 μM). In all sweet-responsive taste buds tested ( n = 11), PDBu elicited burst of action currents. In contrast, PDBu elicited responses in only 4 of 19 sweet-unresponsive taste buds. Inhibition of PKC by bisindolylmaleimide I (0.15 μM) resulted in inhibition of the NC-01 response by ∼75%, whereas the response to sucrose either increased or remained unchanged. These data suggest that activation of PKC is required for the transduction of synthetic sweeteners. To determine whether protein kinase A (PKA) is required for the transduction of sugars, sweet responses were examined in the presence of the membrane-permeant PKA inhibitor H-89 (10 and 19 μM). Surprisingly, H-89 did not decrease responses to either sucrose or NC-01. Instead, responses to both compounds were increased in the presence of the inhibitor. These data suggest that PKA is not required for the transduction of sugars, but may play a modulatory role in both pathways, such as adaptation of the response. We also examined whether Ca2+-calmodulin dependent cAMP phosphodiesterase (CaM-PDE) plays a role in sweet taste transduction, by examining responses to sucrose and synthetic sweeteners in the presence of the CaM-PDE inhibitor W-7 (100 μM). Inhibition resulted in an increase in the response to sucrose, whereas the response to NC-01 remained unchanged. These data suggest that the pathways for sugars and sweeteners are negatively coupled; the Ca2+ that is released from intracellular stores during stimulation with synthetic sweeteners may inhibit the response to sucrose by activation of CaM-PDE.

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Taste Transduction and Modulation

Physiology ◽

10.1152/physiologyonline.1988.3.3.109 ◽

1988 ◽

Vol 3 (3) ◽

pp. 109-112

Author(s):

SS Schiffman

Keyword(s):

Adenosine Receptor ◽

Potassium Salts ◽

Multiple Receptors ◽

Taste Transduction ◽

Taste Cells ◽

Transduction Mechanisms ◽

Sodium And Potassium

The application to the tongue of agents that interact with taste cells can tell us a great deal about transduction mechanisms that mediate taste. Separate pathways for Na+ and K+ appear to be part of the transduction mechanisms for the tastes of sodium and potassium salts. Caffeine and other methyl xanthines can potentiate certain tastes;this enhancement may involve the interaction of caffeine with an adenosine receptor. There is also evidence for glutamate and inosine receptors in addition to multiple receptors for sweet and bitter tastes.

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