A histochemical study of APUD ability in the taste buds of experimentally induced zinc‐deficient mice

Kondô, Isao; Watanabe, Yuichiro; Ito, Yatsuji; Hisada, Taro

doi:10.1111/j.1600-0714.1987.tb00670.x

Cited by 5 publications

(3 citation statements)

References 26 publications

(11 reference statements)

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“…In the taste buds of mice, serotonin histofluorescence was observed only after administration of amine precursors (5-HTP). No histochemical fluorescence was found in untreated animals (Takeda, 1977;Takeda and Kitao, 1980;Suzuki and Takeda, 1983;Kondo et al, 1987). Takeda and his associates concluded that mice taste bud cells had the ability to take up the amine precursor 5-HTP and convert it into serotonin.…”

Section: Discussionmentioning

confidence: 99%

Localization of serotonin in taste buds: A comparative study in four vertebrates

Kim

Roper

1995

J of Comparative Neurology

101

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To investigate monoaminergic synaptic mechanisms in taste buds, we examined taste buds of mice, rats, rabbits, and mudpuppies for the presence of the neurotransmitter candidate, serotonin. Immunocytochemistry revealed serotonin-like immunostaining in cells in mammalian taste buds and Merkel-like basal cells in taste buds of mudpuppies. In untreated mudpuppies and in mammals injected with the precursor to serotonin, L-tryptophan, certain taste cells showed serotonin-like immunoreactivity, although in mammalian taste buds the immunostaining was relatively weak. After pretreating mammals with 5-hydroxytryptophan (5-HTP), the intermediate precursor between L-tryptophan and serotonin, several taste cells showed strong immunoreactivity for serotonin. These findings indicate that mammalian taste cells normally contain serotonin and that taste cells can take up 5-HTP and convert it to serotonin. Immunocytochemistry on wholemount preparations demonstrated that serotonergic cells of mudpuppies (i.e., Merkel-like basal cells) were disposed in a ring at the periphery of taste buds. Similarly, serotonergic cells in mammalian taste buds tended to be located at the periphery of taste buds. Based on the position of serotonergic cells in the taste bud and on recent physiological studies on the actions of serotonin in taste buds, we postulate that serotonin functions as a neuromodulator or neurotransmitter in vertebrate taste buds.

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Section: Discussionmentioning

confidence: 99%

Localization of serotonin in taste buds: A comparative study in four vertebrates

Kim

Roper

1995

J of Comparative Neurology

101

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“…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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“…(Henkin et al, 1967). After this, the studies in animals such as the rat and mouse (Brosvic et al, 1992;Kondo et al, 1987) and doubleblind study of the therapeutic efficacy of zinc gluconate on taste disorder (Yoshida et al, 1991) were performed to examine the relationship between taste acuity and zinc deficiency. The results suggested that zinc deprivation induced decreased gustatory sensitivity and that zinc played an important role in taste.…”

Section: X25 X200mentioning

confidence: 99%