Description of aftertaste perception relies heavily upon the use of these words to convey the taste that is being sensed after a food has been removed from the mouth.
It is the prolonged moderate or strong taste intensities that persist even after a food is no longer present in the mouth that describe aftertaste sensation.
With respect to aftertaste, this type of testing would have to measure the onset of taste perception from the point after which the food was removed from the mouth.
However, the receptor-independent process involves the diffusion of bitter, amphiphilic chemicals like quinine across the taste receptor cell membranes.
Once inside the taste receptor cell, these compounds have been observed to activate intracellular G-proteins and other proteins that are involved in signaling pathways routed to the brain.
[8] The bitter compounds thus activate both the taste receptors on the cell surface, as well as the signaling pathway proteins in the intracellular space.
[9] The combination of both mechanisms leads to an overall longer response of the taste receptor cells to the bitter foods, and aftertaste perception subsequently occurs.
[7][10] These regions were identified when human subjects were exposed to a taste stimulus and their cerebral blood flow measured with magnetic resonance imaging.
Although these regions have been identified as the primary zones for taste processing in the brain, other cortical areas are also activated during eating, as other sensory inputs are being signaled to the cortex.
[2] In it, the insula was observed to be activated for a longer period of time than other sensory processing areas in the brain when the aftertaste profile of aspartame was measured.
Functional magnetic resonance images of the blood flow in the subjects' brains were recorded before and after they swallowed the aspartame solution.
This suggests that the insula may be a primary region for aftertaste sensation because it was activated even after the aspartame solution was no longer present in the mouth.
[14] Recently, GIV3727 (4-(2,2,3-trimethylcyclopentyl) butanoic acid), a chemical that blocks saccharin and acesulfame-K activation of multiple bitter taste receptors has been developed.