Salty sensation, the detection of sodium ions (Na+), is one of the five basic tastes. It is unique among the five basic tastes in that it can be both appetitive and aversive depending on the concentration of Na+. At low salt concentrations (10—100 millimolar, mM) it is generally considered pleasant, but higher concentrations (100—500 mM) are unpleasant. Detection of Na+ has likely been advantageous through human evolution by identifying dietary sources of Na+ while simultaneously avoiding excessive intake to maintain body salt levels within a limited physiologic window. Proper Na+ levels in the body are critical for homeostasis, as neurologic function, cardiac and skeletal muscle contraction, fluid balance, and just about every physiologic process is dependent on proper Na+ concentrations. While salty sensation is primarily elicited by Na+ ions, other monovalent cations, such as potassium (K+) and lithium (Li+) ions, can also be perceived as salty, especially at higher concentrations.
The receptor for saltiness in humans has proven to be elusive, in part because the primary ligand, Na+, is both simple and ubiquitous. Though a definitive receptor has yet to be identified, it has long been known that the appetitive salty taste can be inhibited by amiloride (an organic compound with a guanidinium group containing pyrazine derivative), which has no effect on the aversive taste of high salt concentrations. This suggests that there are two distinct pathways for detecting Na+, and that amiloride inhibits the receptor for the low concentration pathway. Based on the effect of amiloride, the best candidate for the Na+ taste receptor is the epithelial sodium channel (ENaC), as it is a Na+ channel expressed in taste receptor cells (TRCs) and is inhibited by amiloride.
The differential responses to high and low salt concentrations were an interesting paradox, though a mechanism of the switch from appetitive to aversive salt sensation has recently been identified in mouse models. While amiloride inhibits appetitive salt sensing by ENaC-expressing TRCs, high concentrations of Na+, as well as K+ and Li+, cross-activate the bitter and sour receptors on their respective TRCs. Bitter and sour are both aversive, and their receptors are not inhibited by amiloride, so this mechanism explains both the change in the perception and the inability of amiloride to affect aversive salt sensation.
Though the exact identity of the receptors for the TRCs have not been identified, the salty TRCs are thought to signal through the same pathways as the TRCs corresponding to the other basic tastes.
Depolarization of the salty TRCs following a signaling cascade triggered by the taste receptor transmits a signal to afferent neurons. The signal is relayed by the facial nerve (cranial nerve VII) in the anterior two-thirds of the tongue and glossopharyngeal nerve (cranial nerve IX) in the posterior one-third of the tongue. Sensory afferents synapse in the rostral portion of the nucleus of the solitary tract in the brainstem, and are relayed to the thalamus with projections to the primary gustatory cortex.
Salt sensation, along with the other five tastes, decreases with age, which means that salt is not detected at lower concentrations, which may lead to the ingestion of saltier foods. Higher salt intake could exacerbate hypertension in older individuals.
Michael S. Harper
See also: Facial Nerve; Glossopharyngeal Nerve; Supertaster; Taste Aversion; Taste Bud; Taste System; Type 1 Taste Cells; Type III Taste Cells
McLaughlin, Susan K., & Robert F. Margolskee. (1994). The sense of taste. American Scientist, 82(6), 538—545.
Toshi Matsuda & Richard L. Doty. (1995). Age-related taste sensitivity to NaCl: Relationship to tongue locus and stimulation area. Chemical Senses, 20, 283—290.