20.9: The Physiology of Taste
The perception of a salty flavor is facilitated by sodium ions within the oral salivary fluid. Upon consumption of a salty substance, salt crystals disassemble, leading to the liberation of its constituents—Na+ and Cl- ions. These ions subsequently dissolve into the salivary fluid present in the oral cavity. The external environment of the gustatory cells experiences an elevation in Na+ concentration, thereby establishing a potent concentration gradient. This gradient propels the diffusion of Na+ ions into these cells. The influx of Na+ triggers the phenomenon of cell membrane depolarization, subsequently evoking a receptor potential.
Perception of sourness is associated with the detection of hydrogen ion concentration. Analogous to the role of sodium ions in evoking saltiness, hydrogen ions permeate the cellular membrane, resulting in depolarization. Sourness is a tactile response to acids present in our edibles. An increased hydrogen ion concentration in salivary fluid, corresponding to decreased salivary pH, elicits graded potentials within gustatory cells. For instance, citric acid-laden orange juice manifests a sour taste due to its pH value approximating 3. However, it's often sweetened to obscure the inherent sourness.
The salty and sour tastes are induced by cations such as Na+ and H+. The remaining tastes result from food molecules contacting a specific receptor type, a G protein-coupled receptor. This interaction activates a G protein signaling pathway, culminating in the depolarization of the gustatory cell. Sweetness is perceived when gustatory cells detect glucose molecules dissolved in saliva. However, other monosaccharides, such as fructose and artificial sweeteners, including aspartame, saccharin, or sucralose, also stimulate sweet receptors. Each of these compounds has a different binding affinity to the G protein–coupled receptor, which is why some may be perceived as sweeter than glucose.
The bitter taste sensation, akin to sweetness, is triggered when food molecules attach to G protein-coupled receptors. However, the underlying mechanisms vary significantly due to the broad spectrum of bitter-flavored compounds. Some of these substances depolarize or hyperpolarize gustatory cells, whereas others modulate G protein activation within these cells. The specific response elicited is contingent on the molecular constitution of the receptor-bound compound. A prominent class of bitter compounds is represented by alkaloids, nitrogen-rich substances ubiquitously found in plant products like coffee, hops, tannins, tea, and medications such as aspirin. These toxic alkaloids render the plant less prone to microbial invasion and less appealing to herbivorous organisms, suggesting that the function of bitter taste may be principally linked to the activation of protective reflexes, such as the gag reflex, to prevent the ingestion of potential toxins. This means that traditionally consumed bitter foods are usually paired with sweet components to render them palatable (for instance, adding cream and sugar to coffee). Notably, the posterior region of the tongue, possessing the highest concentration of bitter receptors, is an effective site for triggering the gag reflex, providing a mechanism to expel potentially toxic substances.
Umami, frequently described by its savory flavor, is akin to the sweet and bitter tastes and originates from stimulating G-protein-linked receptors by a distinct molecule. This essential molecule, L-glutamate, an amino acid, is the initiator of this receptor. As a result, the umami sensation is frequently experienced when consuming foods rich in protein. Consequently, it's not unexpected that meals containing a high proportion of meat carry a savory descriptor.
Upon activation by taste molecules, gustatory cells initiate a release of neurotransmitters. These neurotransmitters subsequently interact with the dendrites of sensory neurons. Included within these neurons are components of the facial and glossopharyngeal cranial nerves, as well as a segment of the vagus nerve dedicated to the gag reflex. Specifically, the facial nerve connects with taste buds in the tongue's anterior third. In contrast, the glossopharyngeal nerve links with taste buds in the posterior two-thirds of the tongue. Lastly, the vagus nerve communicates with taste buds near the far posterior of the tongue, bordering the pharynx, which showcases heightened sensitivity to harmful stimuli, such as bitterness.
