Taste Buds Essay Example

signals reach the brain, various neural pathways are activated, contributing to digestive function. For instance, tasting food triggers a quick increase in salivation and slight secretion in the stomach. In humans, taste sensitivity varies significantly. Approximately 25% of individuals are classified as "supertasters" who are much more sensitive to bitter and other tastes compared to those with low sensitivity. These differences are genetically determined and result from variations in the number of fungiform papillae, which house taste buds on the tongue.

The distinction between taste papillae and taste buds should be noted. Taste papillae are visible on the tongue as small red dots or raised bumps, mainly at the front of the tongue. These specific papillae are referred to as "fungiform" papillae due to their resemblance to button mushrooms. There are three other types of papillae, namely foliate, circumvallated, and non-gustatory filiform. On the other hand, taste buds are clusters of cells located on these papillae and cannot be observed without magnification. To better understand this, refer to the diagram provided below.

The taste buds, located on top of or on the sides of the papillae, are cellular collections. There are five primary tastes: salt, sour, sweet, bitter, and umami. In regards to salt taste, it is sodium chloride (Na+ Cl-). The receptor cells allow Na+ ions to enter through Na-channels. Specifically, these are referred to as amiloride-sensitive Na+ channels, not to be confused with TTX-sensitive Na+ channels found in nerves and muscles.

The entry of Na+ leads to depolarization, as well as the entry of Ca2+ through voltage-sensitive Ca2+ channels. This results in transmitter release and increased firing in the

primary afferent nerve. Sour taste is caused by acid, which is protons (H+). Recent evidence suggests the existence of an acid-sensing channel called the PKD2L1 channel. This channel belongs to the transient receptor potential channel (TRP) family and is a non-selective cation channel. The activity of PKD2L1 is governed by pH (H+ ion concentration). This discovery challenges previous notions that H+ ions block K+ channels causing depolarization, or that H+ ions enter the cell through ENaC channels. While these mechanisms may still exist, they do not directly contribute to sour perception.

The apical membrane contains receptors (T1R2 + T1R3) that bind glucose, sucrose (a combination of glucose and fructose), and other carbohydrates, resulting in a sweet taste. When these receptors are bound, a G-protein is activated, which in turn activates phospholipase C (PLC-? 2). PLC produces IP3 and diacyl glycerol (DAG), which act as intracellular messengers. These messengers, either directly or indirectly, activate the TRPM5 channel and cause depolarization. Depolarization leads to the influx of Ca2+ through depolarization-activated Ca2+ channels. As a result, neurotransmitter is released, leading to an increase in firing in the primary afferent nerve.
The bitter taste is tasted differently.

The text explains that bitter substances bind to T2R receptors, activating G-proteins and causing PLC activation. This activation leads to the production of second messengers DAG and IP3, which activate TRPM5 and release Ca2+ from internal stores. The increase in Ca2+ levels results in transmitter release, ultimately increasing the firing of the primary afferent nerve. Additionally, the text mentions that umami taste refers to the taste of certain amino acids such as glutamate and aspartate, and it was first discovered by Kikunae

Ikeda in 1909 at the Imperial University of Tokyo.

It has been shown2,3 that the metabotropic glutamate receptor (mGluR4) is responsible for umami taste. When bound to this receptor, a G-protein is activated, resulting in increased intracellular Ca2+. More recently, it has been discovered that umami taste is mediated by the T1R1 + T1R3 receptors4. Activation of these receptors leads to the activation of the non-selective cation channel TRPM5, similar to what occurs with sweet and bitter receptors (i.e. through G-protein, PLC, IP3, and DAG - as mentioned above). Guanosine 5'-monophosphate (GMP) and inosine 5'-monophosphate (IMP) enhance the effect of umami taste by binding to a separate site on the T1R1 receptor.

Monosodium glutamate, which is added to many foods to enhance their taste and is the main ingredient of Soy sauce, stimulates the umami receptors. However, there are also ionotropic glutamate receptors on the tongue, such as the NMDA-receptor, which are linked to ion channels. When these umami compounds or soy sauce activate these receptors, non-selective cation channels open and depolarize the cell. This results in the entry of calcium, release of transmitters, and increased firing in the primary afferent nerve.