Smith D V, van der Klaauw N J
Department of Anatomy, University of Maryland School of Medicine, Baltimore 21201, USA.
Chem Senses. 1995 Oct;20(5):545-57. doi: 10.1093/chemse/20.5.545.
The tastes of salts to humans are complex. NaCl is the most purely salty of all salts, but even this stimulus tastes sweet at low concentrations and somewhat sour at mid-range intensities. Other salts taste significantly sour or bitter in addition to salty. Previous studies have shown that the saltiness of simple halide salts is reduced by adaptation to NaCl, suggesting that a single mechanism might be responsible for the salty taste of these stimuli. In electrophysiological studies in rodents, the response to NaCl is reduced by application to the tongue of the Na(+)-channel blocker amiloride. Organic Na+ salts are more heavily dependent on this amiloride-sensitive transduction component than NaCl, and are generally less salty and more sour. In order to investigate the relationship between NaCl saltiness and that evoked by other salts, we adapted the tongue to distilled H2O and to 0.1 M NaCl and obtained direct magnitude estimates of the taste intensity of 15 organic and inorganic Na+, Li+, K+ and Ca2+ salts, matched for total intensity. Subjects divided these magnitude estimates among the component taste qualities. Adaptation to NaCl abolished the taste of NaCl and LiCl, and eliminated the saltiness of all other salts. The magnitude estimates of the bitterness and sourness of many salts increased after NaCl adaptation. Since recent biophysical data suggest that adaptation in taste receptors may involve whole-cell mechanisms, we propose that saltiness is reduced by NaCl adaptation because it originates in the subset of taste receptors responsive to NaCl. This implies that saltiness is coded within the CNS in cells whose receptive fields include the NaCl-sensitive receptor cells and that the degree to which any salt tastes salty is determined by its ability to drive these receptors. This model proposes, for example, that KCl has a salty component because it stimulates some of the same receptor cells as NaCl, even though the transduction mechanisms for KCl are different than those engaged by NaCl. Adaptation to NaCl blocks the saltiness of KCl and other salts because they stimulate NaCl-sensitive receptor cells.
盐对人类的味觉影响很复杂。氯化钠是所有盐中最纯粹的咸味剂,但即使是这种刺激物在低浓度时也有甜味,在中等强度时会有一点酸味。其他盐除了有咸味外,还明显有酸味或苦味。先前的研究表明,适应氯化钠会降低简单卤化物盐的咸味,这表明单一机制可能负责这些刺激物的咸味感知。在对啮齿动物的电生理研究中,向舌部施加钠离子通道阻滞剂amiloride会降低对氯化钠的反应。有机钠盐比氯化钠更依赖这种对amiloride敏感的转导成分,并且通常咸味更淡、酸味更重。为了研究氯化钠的咸味与其他盐所引发的咸味之间的关系,我们让舌头分别适应蒸馏水和0.1M的氯化钠,并对15种有机和无机的钠离子、锂离子、钾离子和钙离子盐的味觉强度进行了直接的量级估计,这些盐的总强度是匹配的。受试者将这些量级估计分配到不同的味觉品质中。适应氯化钠后,氯化钠和氯化锂的味道消失了,其他所有盐的咸味也消失了。许多盐的苦味和酸味的量级估计在适应氯化钠后增加了。由于最近的生物物理数据表明味觉受体的适应可能涉及全细胞机制,我们提出适应氯化钠会降低咸味是因为咸味起源于对氯化钠有反应的味觉受体子集。这意味着咸味在中枢神经系统中是由其感受野包括对氯化钠敏感的受体细胞的细胞编码的,并且任何一种盐的咸味程度取决于它驱动这些受体的能力。例如,这个模型提出氯化钾有咸味成分是因为它刺激了一些与氯化钠相同的受体细胞,尽管氯化钾的转导机制与氯化钠的不同。适应氯化钠会阻断氯化钾和其他盐的咸味,因为它们刺激对氯化钠敏感的受体细胞。