22: Taste abnormalities

Taste abnormalities


Taste drives appetite and protects people from ingesting poisons. What is called taste in fact is often flavour – a combination of taste with smell (aroma), with texture and other features (e.g. temperature and spiciness).

The sense of taste is mediated by specialized taste buds – oval bodies made up of groups of neuroepithelial and supporting cells (Fig. 22.1). The neuroepithelial cells are rod-shaped with a peripheral hair-like process projecting into the taste pores at the surface of the overlying mucous membrane (Fig. 22.2). There are five basic tastes but they do not appear to be detected by structurally different taste buds:

image Salt taste: mediated via sodium chloride (NaCl) ions. Na+ ions enter the receptor cells via Na+ channels, cause a depolarization, calcium ions enter through voltage-sensitive Ca2 + channels, transmitter release occurs and results in increased firing in the primary afferent nerve.

image Sour taste: mediated by protons (H+), which block potassium channels causing depolarization, Ca2 + entry, transmitter release and increased firing in the primary afferent nerve.

image Sweet taste: receptors bind glucose, which activates adenyl cyclase, thereby increasing cyclic adenosine monophosphate (cAMP), causing phosphorylation of K+ channels, inhibiting them. Depolarization occurs, Ca2 + enters and transmitter is released, increasing firing in the primary afferent nerve.

image Bitter taste: bitter substances cause a second messenger (inositol trisphosphate (IP3)) mediated release of Ca2 + resulting in transmitter release and firing of the primary afferent nerve.

image Umami taste: certain amino acids (e.g. glutamate, aspartate) bind to a glutamate receptor (mGluR4) activating a G-protein, raising intracellular Ca2 +. Glutamate may also stimulate the NMDA (N-methyl-D-aspartate)-receptor, when non-selective cation channels open, and Ca2 + enters, causing transmitter release and increased firing in the primary afferent nerve.

The terminal branches of the nerve fibres subserving taste end in close relationship to these special neuroepithelial cells. Taste buds are found in the mucous membrane of the tongue, soft palate, fauces and pharynx, and, in the newborn, on the lips and cheeks. Taste buds on the tongue are on the fungiform, circumvallate and foliate, but not on the filiform, papillae (Fig. 22.2). Papillae at the front of the tongue have more taste buds compared to the mid-region. Taste buds are also located throughout the oral cavity, in the pharynx, the laryngeal epiglottis and at the entrance of the oesophagus. Sensitivity to all tastes is distributed across the whole tongue and to other regions where there are taste buds (epiglottis, soft palate), but some areas are more responsive to certain tastes than others:

Electrical signals generated in the taste cells transmit information via sensory nerves, which arise from the ganglion cells of branches of cranial nerves:

All three nerves connect in the brainstem in the nucleus solitarius, before proceeding to the thalamus and then to the brain frontal lobe (the insula and the frontal operculum cortex) for the conscious perception of taste, and the hypothalamus, amygdala and insula for the ‘affective’ component of taste – responsible for the behavioural response (e.g. feeding behaviour).


Taste and olfaction are susceptible to the general sensory phenomenon known as adaptation, i.e. the progressive reduction in the appreciation of a stimulus during the course of continual exposure to that stimulus. Taste exhibits almost complete adaptation to a stimulus – perception of a substance fades to almost nothing in seconds. Both taste and olfaction are also susceptible to genetic, hormonal, age and other factors. The cells of the taste buds undergo continual renewal, with a life span of about 10 days, renewal being modulated by nutrition, hormones, and age, and other factors such as drugs and radiation.

Jan 9, 2015 | Posted by in Oral and Maxillofacial Pathology | Comments Off on 22: Taste abnormalities
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