Article Figures & Data
Figures
- Figure 1.
Effect of 5-HT enhancement on taste threshold. Taste psychophysical functions are shown before (filled circles and solid lines) and after (open circles and dotted lines) SSRI. SSRI (paroxetine) administration significantly increased sweet (A) taste sensitivity (p < 0.001) and bitter (B) taste sensitivity (p < 0.0001) but had no effect on salt (C) or sour (D) taste sensitivity. Taste acuity (slope of the line) was unaffected by SSRI administration. Data shown are mean ± SEM.
- Figure 2.
Effect of placebo on taste threshold. Taste psychophysical functions are shown before (filled circles and solid lines) and after (open circles and dotted lines) placebo. Placebo administration did not affect taste sensitivity or acuity for sweet (A), bitter (B), salt (C), or sour (D) taste. Data shown are mean ± SEM.
- Figure 3.
Effect of NA enhancement on taste threshold. Taste psychophysical functions are shown before (filled circles and solid lines) and after (open circles and dotted lines) NARI. A, B, NARI administration had no effect on sweet taste sensitivity (A) but significantly increased bitter taste sensitivity (B) (p < 0.0001). C, D, Salt taste sensitivity was unaffected (C), but sour taste sensitivity was slightly enhanced after NARI administration (D) (p < 0.02). Taste acuity for all tastes was unaffected. Data shown are mean ± SEM.
- Figure 4.
The effects of monoamine manipulation in individuals. A, Taste psychophysical functions in a single individual in response to reboxetine (NARI), which significantly reduced bitter taste threshold in this individual, reducing thresholds by 80% from 0.9 μm to 0.17 μm (p < 0.0001). B, In the same subject, on the same day, reboxetine did not affect salt taste threshold. C, D, When comparing all individual responses before and after drug, monoamine manipulation with paroxetine (parox; SSRI) (C) clearly showed decreases in bitter taste threshold after drug, whereas there was no clear change in salt taste threshold in most individuals with the same drug (D).
- Figure 5.
The relationship between general anxiety level and taste thresholds. There is a significant correlation between anxiety level and bitter (A) and salt (B) baseline taste thresholds, whereas there was no relationship between anxiety and sweet (C) or sour (D) threshold. Each data point is the mean of three baseline taste thresholds and corresponding Spielberger Trait scores.
- Figure 6.
Median split data for bitter and salt threshold showing significantly higher thresholds in the most anxious people. The median value for Spielberger Trait score was 25, and data were split into those above and below this value for comparison. There was a significant difference between the median split groups for bitter threshold (A; 20–25, 26 ± 7 μm; >25, 95 ± 18 μm; p < 0.005) and salt threshold (B; 20–25, 19 ± 3.5 mm; >25, 34 ± 8 mm; p < 0.05), whereas there was no significant difference in sweet threshold (C; 20–25, 30 ± 7 mm; >25, 55 ± 17 mm) or sour threshold (D; 20–25, 11 ± 3 mm; >25, 18 ± 6 mm).
- Figure 7.
Proposed peripheral mechanism of serotonergic modulation of taste. The model is extended from a model of 5-HT as a neurotransmitter in taste buds, proposed by Roper and colleagues (Y. J. Huang et al., 2006; Roper, 2006), and is fully explained in the text. Receptor cells, which contain the necessary molecules for the transduction of sweet, bitter, and umami tastes, are a separate population from the cells that form synapses with gustatory afferents (presynaptic cells) (Clapp et al., 2006; DeFazio et al., 2006). After transduction of a taste stimulus (①), taste cells release ATP (②, open circles). ATP could directly activate gustatory afferents that are known to express ionotropic purinoreceptors but can also activate purinoceptors on presynaptic cells (trapezoid). This results in release of Ca2+ from intracellular stores in presynaptic cells and a subsequent release of 5-HT from presynaptic cells (③, filled circles). We propose an additional possible role of 5-HT. When released from presynaptic cells, 5-HT may also act back through volume transmission on taste cells, and/or gustatory afferents to activate 5-HT receptors (④, shaded diamond) and modulate the response to tastants in the taste cell. Inhibition of 5-HT transporters (SET; ⑤, hatched rectangle) on taste cells by our SSRI administration and the subsequent enhancement of 5-HT signaling could therefore enhance the taste of bitter and sweet substances, as we found. NA could act as either a transmitter released onto gustatory afferents in response to stimulation of presynaptic cells or a modulator of ATP action. Open circles, ATP; filled circles, 5-HT; shaded diamond, 5-HT1A receptor with 5-HT bound; hatched rectangle, SET transporting 5-HT; trapezoid, P2Y2/4 receptor with ATP bound.
Tables
Taste Before placebo After placebo % Change Before SSRI After SSRI % Change Before NARI After NARI % Change Bitter 54 μm 63 μm 16% Increase 30 μm‡ 14 μm† 53% 31 μm‡ 19 μm* 39% (36–79 μm) (41–94 μm) (24–38 μm) (12–19 μm) Decrease† (24 - 39 μm) (15–26 μm) Decrease* Sweet 44 mm 41 mm 7% Decrease 23.4 mm‡ 17 mm*** 27% 26 mm‡ 22 mm 15% (36–53 mm) (34–49 mm) (21–28 mm) (14–19 mm) Decrease*** (22–30 mm) (18–25 mm) Decrease Salt 29 mm 26 mm 10% Decrease 19 mm‡ 19 mm 21 mm‡ 23 mm 9% (21–37 mm) (19–33 mm) (16–21 mm) (18–24 mm) (20–26 mm) Increase Sour 9 mm 9 mm 10 mm 8 mm 20% 9 mm 7 mm* 22% (7–13 mm) (8–13 mm) (8–11 mm) (6–9 mm) Decrease (8–10 mm) (6–8 mm) Decrease* Taste Before placebo (%mm−1) After placebo (%mm−1) Before SSRI (%mm−1) After SSRI (%mm−1) Before NARI (%mm−1) After NARI (%mm−1) Bitter 1.05 1.02 1.1 0.9 1.1 0.9 (0.5–1.6) (0.5–1.6) (0.8–1.3) (0.7–1.2) (0.9–1.4) (0.7–1.1) Sweet 2 2.3 2.1 1.8 2 2.1 (1–3) (1.1–3.5) (1.6–2.6) (1.4–2.2) (1.5–2.5) (1.5–2.6) Salt 1.5 1.4 2.7 2.5 2.4 3.3 (0.3–2.7) (0.3–2.5) (1.8–3.6) (1.7–3.3) (1.7–3.1) (2.2–4.3) Sour 1.2 1.8 1.7 2 2.4 2.2 (0.5–1.9) (0.8–2.8) (1.2–2.1) (1.4–2.5) (1.8–3) (1.6–2.7) -
The value represents the increase in identification (percentage correct response) per millimolar change in concentration. Data shown are means (95% confidence intervals). There were no statistical differences.
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