As molecules reach taste receptors on the microvilli, action-potentials generated through voltage-gated channels will initiate, leading to the excitation of nerve fibres. From there, responses will be carried to the brainstem and be further processed within the brain. The information will eventually translate into taste qualities such as sweet, sour, salty, bitter and umami. Furthermore, each taste quality is specified according to the molecule that binds to the receptor.
Salt taste occurs in the presence of sodium chloride (NaCl ) along with the binding of specific minerals. It is speculated that a sodium channel acts as a receptor for salt. However, researchers are still unsure about the specific receptors that lead to the taste of salt (Chandrashekar et al., 2006). Sour taste is another quality dependent on the detection of ions. When changes in the extracellular pH occur, hydrogen (H+) ions may penetrate taste cells through their tight junctions, contributing to the sour taste (Lindemann, 2001). The PKD2L1 channel, from the TRP family has also been shown to take part in the sour taste sensing (Chandrashekar et al., 2006). Bitter taste is a response to exclusively one, or the combination of: -a variety of bitter compounds binding to T2R G-protein receptors -interaction of bitter compounds with K+ channels or other G proteins -methyl-xanthines permeating the cell and causing an increase in guanidine In the presence of bitter taste, a transient rise of calcium ions (Ca2+) in the cell is noted, although it is not yet known which receptors lead to this change of the membrane potential (Lindemann, 2001). More importantly, the sensing of a bitter taste seems to have evolved and developed multiple ways to decode the sensation, with the intent of avoiding the ingestion of toxic elements. Thus, a variety of distinct reactions lead to the same perception of bitterness (Chandrashekar et al., 2006). Likewise, sweet taste also involves the movement of Ca2+ in and out of the cell. Although the knowledge of the transduction of sweet taste is limited, research has shown that sugars lead to Ca2+ uptake in the cell while non-sugar substances lead to the release of these ions (Lindemann, 2001). Sweet taste receptors respond largely to carbohydrates among other sweet molecules (Lindemann, 2001). The receptors use T1R2 and T1R3 G-proteins, which combine to form sweet receptors …show more content…
However, glutamate alone does not provide a pleasant taste, which is characteristic of umami (McCabe and Rolls, 2007). The taste enhancing quality of umami itself is attributed to the presence of purine 5 '-ribonucleotides, found in decaying meats and other tissues. T1R1 and T1R3 (G-protein channels) taste receptors are also believed to be responsible for the umami taste (Shigemura et al., 2009). However, the perception of umami taste may be due to a result from the combination of both taste and smell (McCabe and Rolls, …show more content…
In terms of odour perception, smell has a more sophisticated process in perception than taste, as there are hundreds of odour receptors (Bakalar, 2012). Thus, the combinations of mixing different tastes and odours can be limitless. (Bakalar, 2012). However, when humans wish to experience a vast variety of flavours, both taste and odour receptors need to be activated, rather than just exclusively one of the two (Bakalar, 2012). In order for us to perceive flavour accurately, both taste and odour processes converge in the anterior insula of the cortex (Bakalar,