Taste receptor

When food or other substances enter the mouth, molecules interact with saliva and are bound to taste receptors in the oral cavity and other locations.

Beyond the papillae, taste receptors are also in the palate and early parts of the digestive system like the larynx and upper esophagus.

They believe this mechanism is evolutionarily adaptive because it helps clear lung infections, but could also be exploited to treat asthma and chronic obstructive pulmonary disease.

[6] The sweet taste receptor (T1R2/T1R3) can be found in various extra-oral organs throughout the human body such as the brain, heart, kidney, bladder, nasal respiratory epithelium and more.

[9] Taste helps to identify toxins, maintain nutrition, and regulate appetite, immune responses, and gastrointestinal motility.

[5] Five basic tastes are recognized today: salty, sweet, bitter, sour, and umami.

[10] In addition, some agents can function as taste modifiers, as miraculin or curculin for sweet or sterubin to mask bitter.

[2] These cells are shown to synapse upon the chorda tympani and glossopharyngeal nerves to send their signals to the brain.

Researchers found a possible explanation for this phenomenon to be a structural change in the ligand binding site of the umami receptor between the sweet taste sensing and non-sensing songbirds.

Common bitter ligands include cycloheximide, denatonium, PROP (6-n-propyl-2-thiouracil), PTC (phenylthiocarbamide), and β-glucopyranosides.

This G protein subunit activates a taste phosphodiesterase and decreases cyclic nucleotide levels.

[26] It has been demonstrated that bitterness receptors (TAS2R) play an important role in an innate immune system of airway (nose and sinuses) ciliated epithelium tissues.

These natural ligands are bacterial markers, for TAS2R38 example: acyl-homoserine lactones[29] or quinolones[30] produced by Pseudomonas aeruginosa.

[27] The innate immune system uses nitric oxide and defensins which are capable of destroying bacteria, and also viruses.

[10] However, proteolyzed forms of ENaC have been shown to function as a human salt taste receptor.

Human sensory studies demonstrated that a compound that enhances proteolyzed ENaC functions to enhance the salty taste of table salt, or sodium chloride, confirming proteolyzed ENaC as the first human salt taste receptor.

[36] CD36 has been localized to the circumvallate and foliate papillae, which are present in taste buds[37] and where lingual lipase is produced, and research has shown that the CD36 receptor binds long chain fatty acids.

[45] However, there are no strong evidences that support any vertebrates are missing the bitter taste receptor genes.

[46] Some mammalian species such as cats and vampire bats have shown inability to taste sweet.

[46] Many studies have shown that the pseudogenization of taste receptors is caused by a deleterious mutation in the open reading frames (ORF).

[46] It is hypothesized that the pseudogenization of Tas1r2 occurred through convergent evolution where carnivorous species lost their ability to taste sweet because of dietary behavior.

[48] In a study, it was found that in all species in the order Carnivora except the panda, the open reading frame was maintained.

[48] In panda, the nonsynonymous to synonymous substitutions ratio was found to be much higher than other species in order Carnivora.

[48] Overall, the loss of function of the a taste receptor is an evolutionary process that occurred due to a dietary change in species.

The diagram above depicts the signal transduction pathway of the sweet taste. Object A is a taste bud, object B is one taste cell of the taste bud, and object C is the neuron attached to the taste cell. I. Part I shows the reception of a molecule. 1. Sugar, the first messenger, binds to a protein receptor on the cell membrane. II. Part II shows the transduction of the relay molecules. 2. G Protein-coupled receptors, second messengers, are activated. 3. G Proteins activate adenylate cyclase, an enzyme, which increases the cAMP concentration. Depolarization occurs. 4. The energy, from step 3, is given to activate the K+, potassium, protein channels.III. Part III shows the response of the taste cell. 5. Ca+, calcium, protein channels is activated.6. The increased Ca+ concentration activates neurotransmitter vesicles. 7. The neuron connected to the taste bud is stimulated by the neurotransmitters.
The diagram depicted above shows the signal transduction pathway of the bitter taste. Bitter taste has many different receptors and signal transduction pathways. Bitter indicates poison to animals. It is most similar to sweet. Object A is a taste bud, object B is one taste cell, and object C is a neuron attached to object B. I. Part I is the reception of a molecule.1. A bitter substance such as quinine, is consumed and binds to G Protein-coupled receptors.II. Part II is the transduction pathway 2. Gustducin, a G protein second messenger, is activated. 3. Phosphodiesterase, an enzyme, is then activated. 4. Cyclic nucleotide, cNMP, is used, lowering the concentration 5. Channels such as the K+, potassium, channels, close.III. Part III is the response of the taste cell. 6. This leads to increased levels of Ca+. 7. The neurotransmitters are activated. 8. The signal is sent to the neuron.
The diagram depicts the signal transduction pathway of the sour or salty taste. Object A is a taste bud, object B is a taste receptor cell within object A, and object C is the neuron attached to object B. I. Part I is the reception of hydrogen ions or sodium ions. 1. If the taste is sour, H+ ions, from an acidic substances, pass through their specific ion channel. Some can go through the Na+ channels. If the taste is salty Na+, sodium, molecules pass through the Na+ channels. Depolarization takes place II. Part II is the transduction pathway of the relay molecules.2. Cation, such as K+, channels are opened. III. Part III is the response of the cell. 3. An influx of Ca+ ions is activated.4. The Ca+ activates neurotransmitters. 5. A signal is sent to the neuron attached to the taste bud.