Serotonergic Agonists Inhibit Calcium-Activated Potassium and Voltage-Dependent Sodium Currents in Rat Taste Receptor Cells

Herness, M. Scott; Chen, Y.

doi:10.1007/s002320001014

Cited by 40 publications

(27 citation statements)

References 36 publications

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“…Current was inhibited 26 Ϯ 5% (n ϭ 9) and 39 Ϯ 4% (n ϭ 11) at Ϫ80 and Ϫ50 mV, respectively. These results are similar to inhibition of outward currents in these cells at these same holding potentials produced by serotonin (17). Similar effects of caffeine could be demonstrated with the use of the potassium channel inhibitors TEA and 4-AP.…”

Section: Resultssupporting

confidence: 72%

Dual actions of caffeine on voltage-dependent currents and intracellular calcium in taste receptor cells

Zhao¹,

Lu²,

Herness

2002

American Journal of Physiology-Regulatory, Integrative and Comp

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-Although the numerous stimuli representing the taste quality of bitterness are known to be transduced through multiple mechanisms, recent studies have suggested an unpredicted complexity of the transduction pathways for individual bitter stimuli. To investigate this notion more thoroughly, a single prototypic bitter stimulus, caffeine, was studied by using patch-clamp and ratiometric imaging techniques on dissociated rat taste receptor cells. At behaviorally relevant concentrations, caffeine produced strong inhibition of outwardly and inwardly rectifying potassium currents. Caffeine additionally inhibited calcium current, produced a weaker inhibition of sodium current, and was without effect on chloride current. Consistent with its effects on voltage-dependent currents, caffeine caused a broadening of the action potential and an increase of the input resistance. Caffeine was an effective stimulus for elevation of intracellular calcium. This elevation was concentration dependent, independent of extracellular calcium or ryanodine, and dependent on intracellular stores as evidenced by thapsigargin treatment. These dual actions on voltageactivated ionic currents and intracellular calcium levels suggest that a single taste stimulus, caffeine, utilizes multiple transduction mechanisms. sensory transduction; bitter; patch clamp; fura 2; ratiometric imaging TASTE RECEPTOR CELLS CONVEY gustatory information from the oral cavity to afferent nerve fibers that, in turn, relay their activation to the central nervous system. Our present understanding of these processes suggests that not only do different transduction mechanisms exist for the varying qualities of taste but multiple mechanisms exist within a taste quality (15,18). Bitter stimuli, in particular, comprise a particularly heterogeneous group of chemically diverse compounds. For example, alkaloids, glucosides, divalent cations, methylated or acetylated carbohydrates, amino acids, and dipeptides are reported to produce bitter sensations in humans. It is not surprising that a number of mechanisms might be required for this wide array of chemically diverse compounds. Moreover, because many bitter compounds are toxic, there exists an evolutionary advantage to evolve multiple mechanisms to sense noxious stimuli. The details of these transduction mechanisms are the subject of this study.Bitter stimuli have been proposed to utilize transduction pathways that include receptor-mediated production or inhibition of second-messenger molecules, modulation of second-messenger molecules by direct interaction with G proteins or degradative enzymes such as phosphodiesterase, or direct block of ion channels. Many bitter stimuli are proposed to be transduced via the gustducin pathway. Gustducin, a G protein expressed in 20-30% of taste receptor cells, shares considerable homology with transducin in photoreceptors (31). By analogy to transducin, the activation of gustducin by a seven-transmembrane receptor is suggested to stimulate phosphodiesterase, thereby lowering cyclic nucleotide...

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Section: Resultssupporting

confidence: 72%

Dual actions of caffeine on voltage-dependent currents and intracellular calcium in taste receptor cells

Zhao¹,

Lu²,

Herness

2002

American Journal of Physiology-Regulatory, Integrative and Comp

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“…It is known that 5-HT release from taste buds is not dependent on calcium influx but on store release (Huang et al, 2005). (4) We propose a serotonergic feedback from presynaptic to receptor cells where 5-HT acts via 5-HT 1A receptors (Delay et al, 1997;Herness and Chen, 1997;Herness and Chen, 2000;Kaya et al, 2004) to modulate bitter and sweet signaling. In some amphibian taste cells, activation of 5-HT 1A receptors is known to increase intracellular calcium levels (Delay et al, 1997), and 5-HT 1A receptors have been shown to affect intracellular calcium in other cell types (Raymond et al, 1992;Khan et al, 1995).…”

Section: Effects Of Monoamine Manipulation On Taste Perceptionmentioning

confidence: 98%

“…The strongest evidence for an involvement of 5-HT and NA in taste signaling is at the level of the taste bud: taste cells from many species express 5-HT (Nada and Hirata, 1975;Kim and Roper, 1995;Clapp et al, 2004), its synthetic enzymes (DeFazio et al, 2006), and its receptors (Delay et al, 1997), and both take up 5-HT (Nagai et al, 1998) and release it in response to stimulation with tastants (Huang et al, 2005). 5-HT and NA affect taste cell excitability by altering ion channel function (Herness and Chen, 1997;Herness and Chen, 2000;Herness et al, 2002). 5-HT modulates responses in primary gustatory neurons (Esakov et al, 1983), possibly through 5-HT 3 receptors (Zhong et al, 1999;Wang et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Human Taste Thresholds Are Modulated by Serotonin and Noradrenaline

Heath

Melichar²,

Nutt³

et al. 2006

J. Neurosci.

176

151

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Circumstances in which serotonin (5-HT) and noradrenaline (NA) are altered, such as in anxiety or depression, are associated with taste disturbances, indicating the importance of these transmitters in the determination of taste thresholds in health and disease. In this study, we show for the first time that human taste thresholds are plastic and are lowered by modulation of systemic monoamines. Measurement of taste function in healthy humans before and after a 5-HT reuptake inhibitor, NA reuptake inhibitor, or placebo showed that enhancing 5-HT significantly reduced the sucrose taste threshold by 27% and the quinine taste threshold by 53%. In contrast, enhancing NA significantly reduced bitter taste threshold by 39% and sour threshold by 22%. In addition, the anxiety level was positively correlated with bitter and salt taste thresholds. We show that 5-HT and NA participate in setting taste thresholds, that human taste in normal healthy subjects is plastic, and that modulation of these neurotransmitters has distinct effects on different taste modalities. We present a model to explain these findings. In addition, we show that the general anxiety level is directly related to taste perception, suggesting that altered taste and appetite seen in affective disorders may reflect an actual change in the gustatory system.

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“…The final events shown, depolarization leading to transmitter release, remain somewhat speculative that serotonin is a paracrine transmitter at 5-HT1A receptors in taste buds. Serotonin may modulate the threshold of sensory receptor cells in the taste bud or alter membrane properties in taste bud cells [138,139]. Indeed, a recent report from L. Donaldson's laboratory shows selective serotonin re-uptake inhibitors alter human taste thresholds for sweet and bitter via a peripheral mechanism [140].…”

Section: Information Flow In the Taste Budmentioning

confidence: 99%

Signal transduction and information processing in mammalian taste buds

Roper

2007

Pflugers Arch - Eur J Physiol

268

215

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The molecular machinery for chemosensory transduction in taste buds has received considerable attention within the last decade. Consequently, we now know a great deal about sweet, bitter, and umami taste mechanisms and are gaining ground rapidly on salty and sour transduction. Sweet, bitter, and umami tastes are transduced by G-protein-coupled receptors. Salty taste may be transduced by epithelial Na channels similar to those found in renal tissues. Sour transduction appears to be initiated by intracellular acidification acting on acidsensitive membrane proteins. Once a taste signal is generated in a taste cell, the subsequent steps involve secretion of neurotransmitters, including ATP and serotonin. It is now recognized that the cells responding to sweet, bitter, and umami taste stimuli do not possess synapses and instead secrete the neurotransmitter ATP via a novel mechanism not involving conventional vesicular exocytosis. ATP is believed to excite primary sensory afferent fibers that convey gustatory signals to the brain. In contrast, taste cells that do have synapses release serotonin in response to gustatory stimulation. The postsynaptic targets of serotonin have not yet been identified. Finally, ATP secreted from receptor cells also acts on neighboring taste cells to stimulate their release of serotonin. This suggests that there is important information processing and signal coding taking place in the mammalian taste bud after gustatory stimulation.

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Serotonergic Agonists Inhibit Calcium-Activated Potassium and Voltage-Dependent Sodium Currents in Rat Taste Receptor Cells

Cited by 40 publications

References 36 publications

Dual actions of caffeine on voltage-dependent currents and intracellular calcium in taste receptor cells

Dual actions of caffeine on voltage-dependent currents and intracellular calcium in taste receptor cells

Human Taste Thresholds Are Modulated by Serotonin and Noradrenaline

Signal transduction and information processing in mammalian taste buds

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