Immunocytochemical localization of serotonin and serotonin transporter (SET) in taste buds of rat

Ren, Yi; Shimada, Keikichi; Shirai, Yasuhito; Fujimiya, Mineko; Saito, Naoaki

doi:10.1016/s0169-328x(99)00253-3

Cited by 26 publications

(24 citation statements)

References 19 publications

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“…There is a report of the serotonin transporter SET in taste buds, but it was not believed to be related to transporter-mediated transmitter release (Ren et al, 1999). Instead, our findings with the PLC␤2 knock-out mice support the last explanation.…”

Section: Discussioncontrasting

confidence: 49%

Mouse Taste Buds Use Serotonin as a Neurotransmitter

et al. 2005

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Synapses between gustatory receptor cells and primary sensory afferent fibers transmit the output signal from taste buds to the CNS. Several transmitter candidates have been proposed for these synapses, including serotonin (5-HT), glutamate, acetylcholine, ATP, peptides, and others, but, to date, none has been unambiguously identified. We used Chinese hamster ovary cells stably expressing 5-HT 2C receptors as biodetectors to monitor 5-HT release from taste buds. When taste buds were depolarized with KCl or stimulated with bitter, sweet, or sour (acid) tastants, serotonin was released. KCl-and acid-induced 5-HT release, but not release attributable to sweet or bitter stimulation, required Ca 2ϩ influx. In contrast, 5-HT release evoked by sweet and bitter stimulation seemed to be triggered by intracellular Ca 2ϩ release. These experiments strongly implicate serotonin as a taste bud neurotransmitter and reveal unexpected transmitter release mechanisms.

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Section: Discussioncontrasting

confidence: 49%

Mouse Taste Buds Use Serotonin as a Neurotransmitter

et al. 2005

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“…(5) Inhibition of 5-HT transporters found on receptor or presynaptic cells (Ren et al, 1999) by SSRI administration (Nagai et al, 1998) would enhance paracrine signaling through 5-HT, resulting in acute changes in taste thresholds to bitter and sweet substances, as we found. This could also possibly explain the taste disturbances (dysgeusia) reported by patients receiving SSRI treatment (Deems et al, 1991).…”

Section: Effects Of Monoamine Manipulation On Taste Perceptionmentioning

confidence: 75%

“…In addition to the localization of 5-HT and its synthetic enzymes, transporters, and receptors in taste cells (Kim and Roper, 1995;Delay et al, 1997;Ren et al, 1999;DeFazio et al, 2006) and its release on stimulation of taste cells (Huang et al, 2005), functional work using zinc-deficient mice (which inhibits the formation of 5-HT in taste cells) showed that the animals had decreased sensitivity to bitter tastes (Kondo et al, 1987). This suggests that 5-HT signaling in taste buds is fundamental to normal taste.…”

Section: -Ht Na and Tastementioning

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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“…To our knowledge ours is the first study to detect quantitatively 5-HT and NA in mouse TRC. Most of the studies conducted hitherto have detected these neurotransmitters immunocytochemically (32) or with fluorescent biosensor probes (29). LA-induced release of 5-HT and NA is mediated via CD36 as SSO curtailed the same.…”

Section: Discussionmentioning

confidence: 99%

Linoleic Acid Induces Calcium Signaling, Src Kinase Phosphorylation, and Neurotransmitter Release in Mouse CD36-positive Gustatory Cells

El-Yassimi

Hichami

Besnard

et al. 2008

Journal of Biological Chemistry

167

136

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We have recently demonstrated that the cells expressing CD36, localized apically on the taste buds of mouse lingual circumvallate papillae, act as gustatory cells. In the present study we isolated these CD36-positive cells from mouse circumvallate papillae and investigated intracellular signaling events, triggered by a long-chain polyunsaturated fatty acid, i.e. linoleic acid (LA). LA induced increases in free intracellular calcium concentrations, [Ca 2؉ ] i , by recruiting calcium from endoplasmic reticulum pool via inositol 1,4,5-triphosphate production followed by calcium influx via opening of store-operated calcium (SOC) channels. LA also induced phosphorylation of Srcprotein-tyrosine kinases (Src-PTKs), particularly of The tongue contains primarily four types of papillae. Filiforms are involved in the somesthesic perception of foods, whereas fungiforms, foliates, and circumvallates, which contain taste buds, are responsible for the chemosensory perception of basic taste modalities (sweet, bitter, salt, sour, umami (4) demonstrated that the addition of a lipase inhibitor diminished the spontaneous preference for triglycerides. These investigators proposed that the lingual lipase, present in the rodent saliva, might release free fatty acids that would be detected by gustatory cells. The immunolocalization of CD36 in the apical side of few TRC in circumvallate papillae (3) is especially adequate for this function since CD36 is known to exhibit a very high affinity for long-chain fatty acids (5). Consistent with this assumption, we have recently provided the first evidence that CD36-positive gustatory cells play a significant role in dietary lipid perception in the mouse (3). Indeed, the CD36 gene inactivation fully abolished the spontaneous preference for long-chain fatty acids observed in wild-type mice (3). It is noteworthy that this effect on feeding behavior is lipid-specific since sweet preference and bitter aversion are not affected in these transgenic mice (3).To further explore whether a sixth taste modality devoted to the "fat" functionally exists in rodents, the downstream signaling events triggered by the free fatty acid/CD36 interaction in gustatory cells must be studied. We have for the first time purified the CD36-positive gustatory cells from mouse CVP and demonstrated that linoleic acid induced increases in [Ca 2ϩ ] i in these cells via CD36 (6). In the present study we have extended these investigations to characterize the mechanisms of action of linoleic acid on calcium signaling/protein phosphorylation, leading to the release of neurotransmitters, which might be implicated in the activation of afferent nerve fibers.

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Immunocytochemical localization of serotonin and serotonin transporter (SET) in taste buds of rat

Cited by 26 publications

References 19 publications

Mouse Taste Buds Use Serotonin as a Neurotransmitter

Mouse Taste Buds Use Serotonin as a Neurotransmitter

Human Taste Thresholds Are Modulated by Serotonin and Noradrenaline

Linoleic Acid Induces Calcium Signaling, Src Kinase Phosphorylation, and Neurotransmitter Release in Mouse CD36-positive Gustatory Cells

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