Genetic and pathological taste variation: what can we learn from animal models and human disease?
Genetic and pathological taste variation: what can we learn from animal models and human disease?
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遗传和病理性味觉变异：我们可以从动物模型和人类疾病中学到什么？
DOI：
10.1002/9780470514511.ch16
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Bartoshuk,LM
中科院分区：
文献类型：
--
作者：
Bartoshuk,LM
对味觉障碍患者的研究（即“自然实验”）表明，教科书中经常出现的旧舌图（例如舌尖甜，背面苦）是错误的。如果他们是正确的，切断支配舌头前部的味觉神经将导致失去品尝甜味等的能力。切断这些神经对日常味觉体验几乎没有影响，因为味觉神经相互抑制。损伤一条神经会破坏它抑制其他神经的能力，而抑制的释放会补偿损伤。这种冗余有时会产生临床成本;抑制的释放会产生味觉幻觉。味觉能力的遗传变异发生在物种之间和物种内部。例如，大约25%的人对各种甜味和苦味化合物相对无反应（非味觉者），而另外25%的人对甜味和苦味化合物的反应异常（超味觉者）。超级味觉者的味蕾数量是非味觉者的四倍，并且具有更小和更密集的菌状乳头。由于味蕾上有痛觉纤维，味觉超敏者对香料的口腔灼烧感有着非同寻常的反应。
The study of patients with taste disorders (i.e. ‘experiments of nature’) suggests that the old tongue maps (e.g. sweet on the tip, bitter on the back) that often appear in textbooks are wrong. If they were correct, severing the taste nerves that innervate the front of the tongue would result in a loss of the ability to taste sweet, etc. This does not occur. Severing these nerves has little effect on everyday taste experience because taste nerves inhibit one another. Damaging one nerve abolishes its ability to inhibit others and the release‐of‐inhibition compensates for the damage. There is sometimes a clinical cost for this redundancy; release‐of‐inhibition can produce taste phantoms. Genetic variation in taste ability occurs across and within species. For example, about 25% of humans are relatively unresponsive to a variety of sweet and bitter compounds (non‐tasters) while another 25% are unusually responsive (supertasters). Supertasters have about four times as many taste buds as non‐tasters and have smaller and more densely packed fungiform papillae. Since there are pain fibres associated with taste buds, supertasters are unusually responsive to the oral burn of spices.