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A histochemical study of APUD ability in the taste buds of experimentally induced zinc‐deficient mice
Author(s) -
Kondo I.,
Watanabe Y.,
Ito Y.,
Hisada T.
Publication year - 1987
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/j.1600-0714.1987.tb00670.x
Subject(s) - monoamine neurotransmitter , taste , zinc , endocrinology , serotonin , taste disorder , medicine , taste bud , zinc deficiency (plant disorder) , chemistry , lingual papilla , biology , biochemistry , receptor , organic chemistry
To explore the relationship between taste acuity and zinc deficiency, a histochemical investigation was made into the taste buds of mice fed a zinc‐deficient diet. Nine weeks after the start of the diet, the average serum zinc level of the mice was 45% lower than that of a control group of mice. Moreover, growth was arrested significantly. Two‐bottle preference tests revealed that the intake ratio of 10 ‐5 M quinine hydrochloride solutions had increased markedly in the zinc‐deficient mice compared with the controls. The circumvallate taste buds showed no morphological changes. Fluorescent histochemical examination showed an uptake of a monoamine precursor (5‐HTP) by the gustatory cells in the zinc‐deficient mice after the 5‐HTP treatment. Upon immunohistological examination, however, no serotonin immunoreactivity appeared in the gustatory cells of the zinc‐deficient mice after the 5‐HTP treatment. These results suggest that zinc‐deficiency may induce hypogeusia and decrease the ability to transform a monoamine precursor to monoamine in the gustatory cells, albeit the monoamine precursor uptake ability is not affected.