Out of all the sensory modalities, olfaction contributes most to the
sensation and perception of flavor processing. Olfaction has two
sensory modalities, orthonasal smell, the detection of odor molecules originating outside the body, and retronasal smell, the detection of odor molecules originating during mastication. It is retronasal smell, whose sensation is felt in the mouth, that contributes to flavor perception. Anthropologically, over human evolution, the shortening of the nasopharynx and other shifts in bone structure suggest a constant improvement of flavor perception capabilities.
After mastication, odor molecules travel through the back of the mouth and up the nasopharynx. The odorants are detected by myriad receptors on the olfactory epithelium.
These receptors respond to a variety of dimensions of chemical
properties. Odor receptors that respond to a dimension within a
molecular receptive range are aggregated by glomeruli in the olfactory bulb. Here, the multi-dimensional nature of odorant stimuli is reduced to two dimensions. This input undergoes edge enhancement, increasing its signal-to-noise ratio by way of lateral inhibition due to mitral cells stemming from the glomerular layer.
This input then reaches the olfactory cortex. Here, Hebbian learning networks allow for recall with partial or weak stimuli, indicating the first stage of conscious perception. Here, connections with the hypothalamus and hippocampus
indicate that olfaction stimuli affect emotion, decision making, and
learning only after significant processing and rudimentary
identification.
Decision making
The
hedonic value of food and its decision making relies on several
concurrent neural processes. The attentional drive to seek and consume
food is modulated by homeostatic
signaling of hunger and satiety. Habit, social interactions, and
nutritional needs affect this signaling. Analysis of non-human primates'
orbitofrontal cortex
suggests decision making is additionally modulated by food
identification, independent of hunger. Activity in the medial
orbitofrontal cortex and anterior singulate suggest that an affective
value is assigned to every food identification. Hedonic pleasure
increases when engaging with food consumption and peaks during satiety.
Impairments in these systems greatly impact the ability to resist the
urge to eat. Imaging studies show that obese
subjects with impairment in dopamine circuits that regulate hedonic
value have issues with reward sensitivity and resist functional
homeostatic signals that normally would prevent overeating.
The consumption of comfort foods
can facilitate feelings of relational connection and belonging, and the
motivation behind pursuing certain foods can be modulated by social
context and environment.
Although the consumption of spicy food can cause pain, people in many cultures ascribe a high hedonic value to it. Psychologist Paul Rozin
puts forth the idea of "benign masochism", a learned tendency that
overrides the typically aversive stimuli because of the risk-taking or
thrill-seeking associated with overcoming pain.
Learned flavor preferences
Learned taste preferences develop as early as in utero, where the fetus is exposed to flavors through amniotic fluid.
Early, innate, preferences exhibit tendencies towards calorie and
protein dense foods. As children grow older, more factors such as peers,
repeated exposures, environments and food availability will modulate
taste preferences.
Describing odors
While naming a flavor or food refines its representation strengthens its recall in memory, the patterns and tendencies in word choice to describe flavor suggests limits to the our perception and communication. In describing the flavor of wine, tasters tend to use words that
function as a combination of visual and texture descriptors, and
references to objects with similar odorant profiles. Color perception heavily influences the word choice describing a
flavor; the color of word's semantic reference is often congruent with
the food's color when the taster can see the food.
Clinical and other academic translations
With
neurogastronomy's roots in neuroscience and psychology, clinical
translation into research in obesity, diabetes, hypertension, eating
disorders, chemoreceptive deficits in cancer treatments, etc. are
explored in clinical neurogastronomy. The term clinical neurogastronomy was coined by neuropsychologist Dan Han, to advocate for quality of life issues and positive clinical outcomes in patient populations. In 2015, Gordon M. Shepherd, Dan Han, Frédéric Morin, Tim McClintock, Bob Perry, Charles Spence, Jehangir Mehta,
Kelsey Rahenkamp, Siddharth Kapoor, Ouita Michel, and Bret Smith formed
the International Society of Neurogastronomy (ISN). ISN is sponsored
by the National Institutes of Health. The inaugural meeting addressed multiple aspects of neurogastronomy
concepts, and focused on its clinical translation including quality of
life issues in cancer treatment and related smell and taste deficits,
then followed by application into treatments for diabetes. Additional
translational efforts included food technology, agriculture, climate
change, and culinary arts.
The tongue is covered with thousands of small bumps called papillae, which are visible to the naked eye. Within each papilla are hundreds of taste buds. The exceptions to this is the filiform papillae that do not contain taste buds. There are between 2000 and 5000 taste buds that are located on the back and front of the tongue. Others
are located on the roof, sides and back of the mouth, and in the throat. Each taste bud contains 50 to 100 taste receptor cells.
Taste receptors in the mouth sense the five basic tastes: sweetness, sourness, saltiness, bitterness, and savoriness (also known as savory or umami). Scientific experiments have demonstrated that these five tastes exist
and are distinct from one another. Taste buds are able to tell different
tastes apart when they interact with different molecules or ions.
Sweetness, savoriness, and bitter tastes are triggered by the binding of
molecules to G protein-coupled receptors on the cell membranes of taste buds. Saltiness and sourness are perceived when alkali metals or hydrogenions meet taste buds, respectively.
As the gustatory system senses both harmful and beneficial
things, all basic tastes bring either caution or craving depending upon
the effect the things they sense have on the body. Sweetness helps to identify energy-rich foods, while bitterness warns people of poisons.
Among humans, taste perception begins to fade during ageing, tongue papillae are lost, and saliva production slowly decreases. Humans can also have distortion of tastes (dysgeusia). Not all mammals share the same tastes: some rodents can taste starch (which humans cannot), cats cannot taste sweetness, and several other carnivores, including hyenas, dolphins, and sea lions, have lost the ability to sense up to four of their ancestral five basic tastes.
Basic tastes
The gustatory system allows animals to distinguish between safe and
harmful food and to gauge different foods' nutritional value. Digestive enzymes
in saliva begin to dissolve food into base chemicals that are washed
over the papillae and detected as tastes by the taste buds. The tongue
is covered with thousands of small bumps called papillae, which are visible to the naked eye. Within each papilla are hundreds of taste buds. The exception to this are the filiform papillae, which do not contain taste buds. There are between 2,000 and 5,000 taste buds that are located on the back and front of the tongue. Others
are located on the roof, sides and back of the mouth, and in the
throat. Each taste bud contains 50 to 100 taste-receptor cells.
The five specific tastes received by taste receptors are saltiness, sweetness, bitterness, sourness, and savoriness (often known by its Japanese name umami, which translates to 'deliciousness').
As of the early 20th century, Western physiologists and
psychologists believed that there were four basic tastes: sweetness,
sourness, saltiness, and bitterness. The concept of a "savory" taste was
not present in Western science at that time, but was postulated in
Japanese research.
One study found that salt and sour taste mechanisms both detect, in different ways, the presence of sodium chloride (salt) in the mouth. Acids are also detected and perceived as sour. The detection of salt is important to many organisms, but especially mammals, as it serves a critical role in ion and water homeostasis in the body. It is specifically needed in the mammalian kidney as an osmotically active compound that facilitates passive re-uptake of water into the blood. Because of this, salt elicits a pleasant taste in most humans.
Sour and salt tastes can be pleasant in small quantities, but in
larger quantities become more and more unpleasant to taste. For sour
taste, this presumably is because the sour taste can signal under-ripe
fruit, rotten meat, and other spoiled foods, which can be dangerous to
the body because of bacteria that grow in such media. Additionally, sour
taste signals acids, which can cause serious tissue damage.
Sweet taste signals the presence of carbohydrates in solution. Since carbohydrates have a very high calorie count (saccharides have many bonds, therefore much energy), they are desirable to the human body, which evolved to seek out the highest-calorie-intake foods. They are used as direct energy (sugars) and storage of energy (glycogen).
Many non-carbohydrate molecules trigger a sweet response, leading to
the development of many artificial sweeteners, including saccharin, sucralose, and aspartame. It is still unclear how these substances activate the sweet receptors and what adaptative significance this has had.
The savory taste (known in Japanese as umami), identified by Japanese chemist Kikunae Ikeda, signals the presence of the amino acidL-glutamate. The amino acids in proteins are used in the body to build muscles and organs, and to transport molecules (hemoglobin), antibodies, and the organic catalysts known as enzymes.
These are all critical molecules, and it is important to have a steady
supply of amino acids; consequently, savory tastes trigger a pleasurable
response, encouraging the intake of peptides and proteins.
Pungency (piquancy or hotness) had traditionally been considered a sixth basic taste. In 2015, researchers suggested a new basic taste of fatty acids called "fat taste", although "oleogustus" and "pinguis" have both been proposed as alternate terms.
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.
Sweetness, usually regarded as a pleasurable sensation, is produced by the presence of sugars and substances that mimic sugar. Sweetness may be connected to aldehydes and ketones, which contain a carbonyl group. Sweetness is detected by a variety of G protein coupled receptors (GPCR) coupled to the G proteingustducin found on the taste buds.
At least two different variants of the "sweetness receptors" must be
activated for the brain to register sweetness. Compounds the brain
senses as sweet are compounds that can bind with varying bond strength
to two different sweetness receptors. These receptors are T1R2+3
(heterodimer) and T1R3 (homodimer), which account for all sweet sensing
in humans and animals.
Taste detection thresholds for sweet substances are rated relative to sucrose, which has an index of 1. The average human detection threshold for sucrose is 10 millimoles per liter. For lactose it is 30 millimoles per liter, with a sweetness index of 0.3, and 5-nitro-2-propoxyaniline 0.002 millimoles per liter. "Natural" sweeteners such as saccharides activate the GPCR, which releases gustducin. The gustducin then activates the molecule adenylate cyclase, which catalyzes the production of the molecule cAMP,
or adenosine 3', 5'-cyclic monophosphate. This molecule closes
potassium ion channels, leading to depolarization and neurotransmitter
release. Synthetic sweeteners such as saccharin activate different GPCRs and induce taste receptor cell depolarization by an alternate pathway.
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 acidic substances, pass through H+ 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.
Sourness is the taste that describes acidity. The sourness of substances is rated relative to dilute hydrochloric acid, which has a sourness index of 1. By comparison, tartaric acid has a sourness index of 0.7, citric acid an index of 0.46, and carbonic acid an index of 0.06.
Sour taste is detected by a small subset of cells that are
distributed across all taste buds called Type III taste receptor cells.
H+ ions (protons) that are abundant in sour substances can directly enter the Type III taste cells through a proton channel. This channel was identified in 2018 as otopetrin 1 (OTOP1). The transfer of positive charge into the cell can itself trigger an
electrical response. Some weak acids such as acetic acid can also
penetrate taste cells; intracellular hydrogen ions inhibit potassium
channels, which normally function to hyperpolarize the cell. By a
combination of direct intake of hydrogen ions through OTOP1 ion channels
(which itself depolarizes the cell) and the inhibition of the
hyperpolarizing channel, sourness causes the taste cell to fire action
potentials and release neurotransmitter.
"Saltiness" redirects here. For saltiness in water, see Salinity.
Saltiness taste seems to have two components: a low-salt signal and a
high-salt signal. The low-salt signal causes a sensation of
deliciousness, while the high-salt signal typically causes the sensation
of "too salty".
The low-salt signal is understood to be caused by the epithelial sodium channel (ENaC), which is composed of three subunits. ENaC in the taste cells allow sodium cations to enter the cell. This on its own depolarizes the cell, and opens voltage-dependent calcium channels, flooding the cell with positive calcium ions and leading to neurotransmitter release. ENaC can be blocked by the drug amiloride
in many mammals, especially rats. The sensitivity of the low-salt taste
to amiloride in humans is much less pronounced, leading to conjecture
that there may be additional low-salt receptors besides ENaC to be
discovered.
A number of similar cations also trigger the low salt signal. The size of lithium and potassium ions most closely resemble those of sodium, and thus the saltiness is most similar. In contrast, rubidium and caesium ions are far larger, so their salty taste differs accordingly. The saltiness of substances is rated relative to sodium chloride (NaCl), which has an index of 1. Potassium, as potassium chloride (KCl), is the principal ingredient in salt substitutes and has a saltiness index of 0.6.
Other monovalentcations, e.g. ammonium (NH4+), and divalent cations of the alkali earth metal group of the periodic table, e.g. calcium (Ca2+),
ions generally elicit a bitter rather than a salty taste even though
they, too, can pass directly through ion channels in the tongue,
generating an action potential.
But the chloride of calcium is saltier and less bitter than potassium
chloride, and is commonly used in pickle brine instead of KCl.
The high-salt signal is poorly understood. This signal is not
blocked by amiloride in rodents. Sour and bitter cells trigger on high
chloride levels, but the specific receptor is unidentified.
The
diagram depicted above shows the signal transduction pathway of the
bitter taste. Bitter taste has many different receptors and signal
transduction pathways. 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.
Bitterness is of interest to those who study evolution, as well as various health researchers since a large number of natural bitter compounds are known to be toxic.
The ability to detect bitter-tasting, toxic compounds at low thresholds
is considered to provide an important protective function. Plant leaves often contain toxic compounds, and among leaf-eating
primates there is a tendency to prefer immature leaves, which tend to
be higher in protein and lower in fiber and poisons than mature leaves. Amongst humans, various food processing techniques are used worldwide to detoxify otherwise inedible foods and make them palatable. Furthermore, the use of fire, changes in diet, and avoidance of toxins
has led to neutral evolution in human bitter sensitivity. This has
allowed several loss of function mutations that has led to a reduced
sensory capacity towards bitterness in humans when compared to other
species.
The threshold for stimulation of bitter taste by quinine averages a concentration of 8 μM (8 micromolar). The taste thresholds of other bitter substances are rated relative to quinine, which is thus given a reference index of 1. For example, brucine
has an index of 11, is thus perceived as intensely more bitter than
quinine, and is detected at a much lower solution threshold. The most bitter natural substance is amarogentin, a compound present in the roots of the plant Gentiana lutea, and the most bitter substance known is the synthetic chemical denatonium, which has an index of 1,000. It is used as an aversive agent (a bitterant)
that is added to toxic substances to prevent accidental ingestion. It
was discovered accidentally in 1958 during research on a local
anesthetic by T. & H. Smith of Edinburgh, Scotland.
Research has shown that TAS2Rs (taste receptors, type 2, also known as T2Rs) such as TAS2R38 coupled to the G proteingustducin are responsible for the human ability to taste bitter substances. They are identified not only by their ability to taste for certain "bitter" ligands, but also by the morphology of the receptor itself (surface bound, monomeric). The TAS2R family in humans is thought to comprise about 25 different
taste receptors, some of which can recognize a wide variety of
bitter-tasting compounds. Over 670 bitter-tasting compounds have been identified, on a bitter database, of which over 200 have been assigned to one or more specific receptors. It is speculated that the selective constraints on the TAS2R family
have been weakened due to the relatively high rate of mutation and
pseudogenization. Researchers use two synthetic substances, phenylthiocarbamide (PTC) and 6-n-propylthiouracil (PROP) to study the genetics
of bitter perception. These two substances taste bitter to some people,
but are virtually tasteless to others. Among the tasters, some are
so-called "supertasters"
to whom PTC and PROP are extremely bitter. The variation in sensitivity
is determined by two common alleles at the TAS2R38 locus. This genetic variation in the ability to taste a substance has been a source of great interest to those who study genetics.
Gustducin is made of three subunits. When it is activated by the GPCR, its subunits break apart and activate phosphodiesterase,
a nearby enzyme, which in turn converts a precursor within the cell
into a secondary messenger, which closes potassium ion channels. Also, this secondary messenger can stimulate the endoplasmic reticulum
to release Ca2+ which contributes to depolarization. This leads to a
build-up of potassium ions in the cell, depolarization, and
neurotransmitter release. It is also possible for some bitter tastants
to interact directly with the G protein, because of a structural
similarity to the relevant GPCR.
The most bitter substance known to date – oligoporin D – stimulates the bitter taste receptor type TAS2R46 at the lowest concentrations 100 nM (0.1 micromolar, approx. 63 millionths of a gram/liter).
Savoriness, or umami, is an appetitive taste. It can be tasted in soy sauce, meat, dashi and consomme. Umami, a loanword from Japanese meaning "good flavor" or "good taste", which is similar to the word "savory" that comes from the French for "tasty". Umami (旨味) is considered fundamental to many East Asian cuisines, such as Japanese cuisine. It dates back to the use of fermented fish sauce: garum in ancient Rome and ge-thcup or koe-cheup in ancient China.
Umami was first studied in 1907 by Ikeda isolating dashi taste, which he identified as the chemical monosodium glutamate (MSG) MSG is a sodium salt that produces a strong savory taste, especially combined with foods rich in nucleotides such as meats, fish, nuts, and mushrooms.
Some savory taste buds respond specifically to glutamate in the
same way that "sweet" ones respond to sugar. Glutamate binds to a
variant of G protein coupled glutamate receptors.L-glutamate may bond to a type of GPCR known as a metabotropic glutamate receptor (mGluR4) which causes the G-protein complex to activate the sensation of umami.
Perceptual independence from salty and sweet taste
There
are doubts regarding whether umami is different from salty taste, as
standalone glutamate(glutamic acid) without table salt ions(Na+), is
perceived as sour, salt taste blockers reduce discrimination between
monosodium glutamate and sucrose in rodents, since sweet and umami
tastes share a taste receptor subunit; and part of the human population
cannot tell apart umami from salty.
If umami doesn't have perceptual independence, it could be
classified with other tastes like fat, carbohydrate, metallic, and
calcium, which can be perceived at high concentrations but may not offer
a prominent taste experience.
Measuring the degree to which a substance presents one basic taste
can be achieved in a subjective way by comparing its taste to a
reference substance.
Sweetness is subjectively measured by comparing the threshold
values, or level at which the presence of a dilute substance can be
detected by a human taster, of different sweet substances. Substances are usually measured relative to sucrose, which is usually given an arbitrary index of 1 or 100. Rebaudioside A is 100 times sweeter than sucrose; fructose is about 1.4 times sweeter; glucose, a sugar found in honey and vegetables, is about three-quarters as sweet; and lactose, a milk sugar, is one-half as sweet.
The sourness of a substance can be rated by comparing it to very dilute hydrochloric acid (HCl).
Relative saltiness can be rated by comparison to a dilute salt solution.
Quinine, a bitter medicinal found in tonic water, can be used to subjectively rate the bitterness of a substance. Units of dilute quinine hydrochloride (1 g in 2000 mL of water) can be
used to measure the threshold bitterness concentration, the level at
which the presence of a dilute bitter substance can be detected by a
human taster, of other compounds. More formal chemical analysis, while possible, is difficult.
There may not be an absolute measure for pungency, though there
are tests for measuring the subjective presence of a given pungent
substance in food, such as the Scoville scale for capsaicine in peppers or the Pyruvate scale for pyruvates in garlics and onions.
Functional structure
Taste buds and papillae of the human tongueTaste receptors of the human tongueSignal transduction of taste receptors
Taste is a form of chemoreception which occurs in the specialised taste receptors
in the mouth. To date, there are five different types of taste these
receptors can detect which are recognized: salt, sweet, sour, bitter,
and umami. Each type of receptor has a different manner of sensory transduction:
that is, of detecting the presence of a certain compound and starting
an action potential which alerts the brain. It is a matter of debate
whether each taste cell is tuned to one specific tastant or to several;
Smith and Margolskee claim that "gustatory neurons typically respond to
more than one kind of stimulus, [a]lthough each neuron responds most
strongly to one tastant". Researchers believe that the brain interprets
complex tastes by examining patterns from a large set of neuron
responses. This enables the body to make "keep or spit out" decisions
when there is more than one tastant present. "No single neuron type
alone is capable of discriminating among stimuli or different qualities,
because a given cell can respond the same way to disparate stimuli." As well, serotonin
is thought to act as an intermediary hormone which communicates with
taste cells within a taste bud, mediating the signals being sent to the
brain. Receptor molecules are found on the top of microvilli of the taste cells.
Sweetness
Sweetness is produced by the presence of sugars, some proteins, and other substances such as alcohols like anethol, glycerol and propylene glycol, saponins such as glycyrrhizin, artificial sweeteners (organic compounds with a variety of structures), and lead compounds such as lead acetate. It is often connected to aldehydes and ketones, which contain a carbonyl group. Many foods can be perceived as sweet regardless of their actual sugar content. For example, some plants such as liquorice, anise or stevia can be used as sweeteners. Rebaudioside A is a steviol glycoside
coming from stevia that is 200 times sweeter than sugar. Lead acetate
and other lead compounds were used as sweeteners, mostly for wine, until
lead poisoning became known. Romans used to deliberately boil the must inside of lead vessels to make a sweeter wine.
Sweetness is detected by a variety of G protein-coupled receptors coupled to a G protein that acts as an intermediary in the communication between taste bud and brain, gustducin. These receptors are T1R2+3 (heterodimer) and T1R3 (homodimer), which account for sweet sensing in humans and other animals.
Saltiness
Saltiness is a taste produced best by the presence of cations (such as Na+ , K+ or Li+ ) and is directly detected by cation influx into glial like cells via leak channels causing depolarisation of the cell.
Other monovalent cations, e.g., ammonium, NH+ 4, and divalent cations of the alkali earth metal group of the periodic table, e.g., calcium, Ca2+ , ions, in general, elicit a bitter rather than a salty taste even though they, too, can pass directly through ion channels in the tongue.
Sourness
Sourness is acidity, and, like salt, it is a taste sensed using ion channels. Undissociated acid diffuses across the plasma membrane of a presynaptic cell, where it dissociates in accordance with Le Chatelier's principle.
The protons that are released then block potassium channels, which
depolarise the cell and cause calcium influx. In addition, the taste
receptor PKD2L1 has been found to be involved in tasting sour.
Bitterness
Research has shown that TAS2Rs (taste receptors, type 2, also known as T2Rs) such as TAS2R38 are responsible for the ability to taste bitter substances in vertebrates. They are identified not only by their ability to taste certain bitter
ligands, but also by the morphology of the receptor itself (surface
bound, monomeric).
Glutamic acid binds to a variant of the G protein-coupled receptor, producing a savory taste.
Further sensations and transmission
The tongue can also feel other sensations not generally included in the basic tastes. These are largely detected by the somatosensory system. In humans, the sense of taste is conveyed via three of the twelve cranial nerves. The facial nerve (VII) carries taste sensations from the anterior two thirds of the tongue, the glossopharyngeal nerve (IX) carries taste sensations from the posterior one third of the tongue while a branch of the vagus nerve (X) carries some taste sensations from the back of the oral cavity.
The trigeminal nerve
(cranial nerve V) provides information concerning the general texture
of food as well as the taste-related sensations of peppery or hot (from spices).
This particular sensation, called chemesthesis,
is not a taste in the technical sense, because the sensation does not
arise from taste buds, and a different set of nerve fibers carry it to
the brain. Foods like chili peppers activate nerve fibers directly; the
sensation interpreted as "hot" results from the stimulation of
somatosensory (pain/temperature) fibers on the tongue. Many parts of the
body with exposed membranes but no taste sensors (such as the nasal
cavity, under the fingernails, surface of the eye or a wound) produce a similar sensation of heat when exposed to hotness agents.
Coolness
Some substances activate cold trigeminal receptors even when not at low temperatures. This "fresh" or "minty" sensation can be tasted in peppermint and spearmint and is triggered by substances such as menthol, anethol, ethanol, and camphor. Caused by activation of the same mechanism that signals cold, TRPM8 ion channels on nerve cells, unlike the actual change in temperature described for sugar substitutes, this coolness is only a perceived phenomenon.
Numbness
Both Chinese and Batak Toba cooking include the idea of 麻 (má) or mati rasa, a tingling numbness caused by spices such as Sichuan pepper. The cuisines of Sichuan province in China and of the Indonesian province of North Sumatra often combine this with chili pepper to produce a 麻辣 málà, "numbing-and-hot", or "mati rasa" flavor. Typical in northern Brazilian cuisine, jambu is an herb used in dishes like tacacá.
These sensations, although not taste, fall into a category of chemesthesis.
Astringency
Some foods, such as unripe fruits, contain tannins or calcium oxalate that cause an astringent or puckering sensation of the mucous membrane of the mouth. Examples include tea, red wine, or rhubarb. Other terms for the astringent sensation are "dry", "rough", "harsh"
(especially for wine), "tart" (normally referring to sourness),
"rubbery", "hard" or "styptic".
Metallicness
A metallic taste may be caused by food and drink, certain medicines or amalgam dental fillings. It is generally considered an off flavor when present in food and drink. A metallic taste may be caused by galvanic
reactions in the mouth. In the case where it is caused by dental work,
the dissimilar metals used may produce a measurable current. Some artificial sweeteners are perceived to have a metallic taste, which is detected by the TRPV1 receptors. Many people consider blood to have a metallic taste.A metallic taste in the mouth is also a symptom of various medical
conditions, in which case it may be classified under the symptoms dysgeusia or parageusia, referring to distortions of the sense of taste, and can be caused by medication, including saquinavir, zonisamide, and various kinds of chemotherapy, as well as occupational hazards, such as working with pesticides.
Fat taste
Recent research reveals a potential taste receptor called the CD36 receptor. CD36 was targeted as a possible lipid taste receptor because it binds to fat molecules (more specifically, long-chain fatty acids), and it has been localized to taste bud cells (specifically, the circumvallate and foliate papillae). There is a debate over whether we can truly taste fats, and supporters
of human ability to taste free fatty acids (FFAs) have based the
argument on a few main points: there is an evolutionary advantage to
oral fat detection; a potential fat receptor has been located on taste
bud cells; fatty acids evoke specific responses that activate gustatory neurons, similar to other currently accepted tastes; and, there is a physiological response to the presence of oral fat. Although CD36 has been studied primarily in mice, research examining human subjects' ability to taste fats found that those with high levels of CD36 expression were more sensitive to tasting fat than were those with low levels of CD36 expression; this study points to a clear association between CD36 receptor quantity and the ability to taste fat.
Other possible fat taste receptors have been identified. G protein-coupled receptorsfree fatty acid receptor 4 (also termed GPR120) and to a much lesser extent Free fatty acid receptor 1 (also termed GPR40) have been linked to fat taste, because their absence resulted in reduced preference to two types of fatty acid (linoleic acid and oleic acid), as well as decreased neuronal response to oral fatty acids.
Monovalent cation channel TRPM5 has been implicated in fat taste as well, but it is thought to be involved primarily in downstream processing of
the taste rather than primary reception, as it is with other tastes such
as bitter, sweet, and savory.
Proposed alternate names to fat taste include oleogustus and pinguis, although these terms are not widely accepted. The main form of fat that is commonly ingested is triglycerides,
which are composed of three fatty acids bound together. In this state,
triglycerides are able to give fatty foods unique textures that are
often described as creaminess. But this texture is not an actual taste.
It is only during ingestion that the fatty acids that make up
triglycerides are hydrolysed into fatty acids via lipases. The taste is
commonly related to other, more negative, tastes such as bitter and sour
due to how unpleasant the taste is for humans. Richard Mattes, a
co-author of the study, explained that low concentrations of these fatty
acids can create an overall better flavor in a food, much like how
small uses of bitterness can make certain foods more rounded. A high
concentration of fatty acids in certain foods is generally considered
inedible. To demonstrate that individuals can distinguish fat taste from other
tastes, the researchers separated volunteers into groups and had them
try samples that also contained the other basic tastes. Volunteers were
able to separate the taste of fatty acids into their own category, with
some overlap with savory samples, which the researchers hypothesized was
due to poor familiarity with both. The researchers note that the usual
"creaminess and viscosity we associate with fatty foods is largely due
to triglycerides", unrelated to the taste; while the actual taste of fatty acids is not pleasant. Mattes described the taste as "more of a warning system" that a certain food should not be eaten.
There are few regularly consumed foods rich in fat taste, due to
the negative flavor that is evoked in large quantities. Foods whose
flavor to which fat taste makes a small contribution include olive oil
and fresh butter, along with various kinds of vegetable and nut oils.
Heartiness
Kokumi (/koʊkuːmi/, Japanese: kokumi (コク味) from koku (こく))
is translated as "heartiness", "full flavor" or "rich" and describes
compounds in food that do not have their own taste, but enhance the
characteristics when combined.
Alongside the five basic tastes of sweet, sour, salt, bitter and savory, kokumi
has been described as something that may enhance the other five tastes
by magnifying and lengthening the other tastes, or "mouthfulness". Garlic is a common ingredient to add flavor used to help define the characteristic kokumi flavors.
Calcium-sensing receptors (CaSR) are receptors for kokumi substances which, applied around taste pores, induce an increase in the intracellular Ca concentration in a subset of cells. This subset of CaSR-expressing taste cells are independent from the influenced basic taste receptor cells. CaSR agonists directly activate the CaSR on the surface of taste cells
and integrated in the brain via the central nervous system. A basal
level of calcium, corresponding to the physiological concentration, is
necessary for activation of the CaSR to develop the kokumi sensation.
Calcium
The distinctive taste of chalk has been identified as the calcium component of that substance. In 2008, geneticists discovered a calcium receptor on the tongues of mice. The CaSR receptor is commonly found in the gastrointestinal tract, kidneys, and brain.
Along with the "sweet" T1R3 receptor, the CaSR receptor can detect
calcium as a taste. Whether the perception exists or not in humans is
unknown.
Temperature
Temperature
can be an essential element of the taste experience. Heat can
accentuate some flavors and decrease others by varying the density and
phase equilibrium of a substance. Food and drink that—in a given
culture—is traditionally served hot is often considered distasteful if
cold, and vice versa. For example, alcoholic beverages, with a few
exceptions, are usually thought best when served at room temperature or
chilled to varying degrees, but soups—again, with exceptions—are usually
only eaten hot. A cultural example are soft drinks. In North America it is almost always preferred cold, regardless of season.
Starchiness
A 2016 study suggested that humans can taste starch (specifically, a glucoseoligomer) independently of other tastes such as sweetness, without suggesting an associated chemical receptor.
Nerve supply and neural connections
Active brain areas in taste perceptionThis
diagram linearly (unless otherwise mentioned) tracks the projections of
all known structures that allow for taste to their relevant endpoints
in the human brain.
The lingual nerve (trigeminal, not shown in diagram) is deeply
interconnected with the chorda tympani in that it provides all other
sensory info from the anterior two-thirds of the tongue. This info is processed separately (nearby) in the rostral lateral subdivision of the nucleus of the solitary tract (NST).
The NST receives input from the amygdala (regulates oculomotor nuclei output), bed nuclei of stria terminalis,
hypothalamus, and prefrontal cortex. The NST is the topographical map
that processes gustatory and sensory (temp, texture, etc.) info.
The reticular formation (includes Raphe nuclei responsible for
serotonin production) is signaled to release serotonin during and after a
meal to suppress appetite. Similarly, salivary nuclei are signaled to decrease saliva secretion.
The frontal operculum is speculated to be the memory and association hub for taste.
The insula cortex aids in swallowing and gastric motility.
Taste in insects
Insects
taste using small hair-like structures called taste sensilla,
specialized sensory organs located on various body parts such as the
mouthparts, legs, and wings. These sensilla contain gustatory receptor
neurons (GRNs) sensitive to a wide range of chemical stimuli.
Insects respond to sugar, bitter, acid, and salt tastes. However,
their taste spectrum extends to include water, fatty acids, metals,
carbonation, RNA, ATP, and pheromones. Detecting these substances is
vital for behaviors like feeding, mating, and oviposition.
Invertebrates' ability to taste these compounds is fundamental to
their survival and provides insights into the evolution of sensory
systems. This knowledge is crucial for understanding insect behavior and
has applications in pest control and pollination biology.
A supertaster is a person whose sense of taste is significantly more
sensitive than most. The cause of this heightened response is likely, at
least in part, due to an increased number of fungiform papillae. Studies have shown that supertasters require less fat and sugar in
their food to get the same satisfying effects. These people tend to
consume more salt than others. This is due to their heightened sense of
the taste of bitterness, and the presence of salt drowns out the taste
of bitterness.
Aftertastes arise after food has been swallowed. An aftertaste can differ from the food it follows. Medicines and tablets may also have a lingering aftertaste, as they can contain certain artificial flavor compounds, such as aspartame (artificial sweetener).
An acquired taste often refers to an appreciation for a food or
beverage that is unlikely to be enjoyed by a person who has not had
substantial exposure to it, usually because of some unfamiliar aspect of
the food or beverage, including bitterness, a strong or strange odor,
taste, or appearance.
Clinical significance
Patients with Addison's disease, pituitary insufficiency, or cystic fibrosis sometimes have a hyper-sensitivity to the five primary tastes.
In the West, Aristotle postulated in c. 350BC that the two most basic tastes were sweet and bitter. He was one of the first persons to develop a list of basic tastes.
Research
The receptors for the basic tastes of bitter, sweet and savory have been identified. They are G protein-coupled receptors. The cells that detect sourness have been identified as a subpopulation that express the protein PKD2L1, and The responses are mediated by an influx of protons into the cells. As of 2019, molecular mechanisms for each taste appear to be different, although all taste perception relies on activation of P2X purinoreceptors on sensory nerves.
