CHAPTER 11 Smell & Taste

221

CLINICAL BOX 111

Abnormalities in Odor Detection
Anosmia (inability to smell) and hyposmia or hypesthesia
(diminished olfactory sensitivity) can result from simple nasal
congestion or nasal polyps. It may also be a sign of a more serious problem such as damage to the olfactory nerves due to
fractures of the cribriform plate or head trauma, tumors such
as neuroblastomas or meningiomas, and respiratory tract infections (such as abscesses). Congenital anosmia is a rare disorder in which an individual is born without the ability to smell.
Prolonged use of nasal decongestants can also lead to anosmia
and damage to the olfactory nerves is often seen in patients
with Alzheimer disease. According to the National Institutes
of Health, 12% of the North American population under the
age of 65 experiences a significant degree of loss of smell. However, aging is associated with abnormalities in smell sensation;
50% of individuals between the ages of 65 and 80 and >75%
of those over the age of 80 have an impaired ability to identify smells. Because of the close relationship between taste and
smell, anosmia is associated with a reduction in taste sensitivity (hypogeusia). Anosmia is generally permanent in cases in
which the olfactory nerve or other neural elements in the olfactory neural pathway are damaged. In addition to not being

ADAPTATION
It is common knowledge that when one is continuously
exposed to even the most disagreeable odor, perception of the
odor decreases and eventually ceases. This sometimes beneficent phenomenon is due to the fairly rapid adaptation, or
desensitization, that occurs in the olfactory system. Adaptation in the olfactory system occurs in several stages. The first
step may be mediated by a calcium-binding protein (calcium/
calmodulin) that binds to the receptor channel protein to
lower its affinity for cyclic nucleotides. The next step is called
short-term adaptation, which occurs in response to cAMP and
implicates a feedback pathway involving calcium/calmodulindependent protein kinase II acting on adenylyl cyclase. The
next step is called long-term adaptation, which includes activation of guanylyl cyclase and cGMP production. A Na+/Ca2+
exchanger to restore ion balance also contributes to long-term
adaptation.

TASTE
TASTE BUDS
The specialized sense organ for taste (gustation) consists of
approximately 10,000 taste buds, which are ovoid bodies measuring 5070 m. There are four morphologically distinct types
of cells within each taste bud: basal cells, dark cells, light cells,

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able to experience the enjoyment of pleasant aromas and a full

spectrum of tastes, individuals with anosmia are at risk because
they are not able to detect the odor from dangers such as gas
leaks, fire, and spoiled food. Hyperosmia (enhanced olfactory
sensitivity) is less common than loss of smell, but pregnant
women commonly become oversensitive to smell. Dysosmia
(distorted sense of smell) can be caused by several disorders
including sinus infections, partial damage to the olfactory
nerves, and poor dental hygiene.

THERAPEUTIC HIGHLIGHTS
Quite often anosmia is a temporary condition due to
sinus infection or a common cold, but it can be permanent if caused by nasal polyps or trauma. Antibiotics
can be prescribed to reduce the inflammation caused by
polyps and improve the ability to smell. In some cases,
surgery is performed to remove the nasal polyps. Topical
corticosteroids have also been shown to be effective in
reversing the loss of smell due to nasal and sinus diseases.

and intermediate cells (Figure 115). The latter three cell types
are also referred to as Type I, II, and III taste cells. They are
the sensory neurons that respond to taste stimuli or tastants.
Each taste bud has between 50 and 100 taste cells. The three cell
types may represent various stages of differentiation of developing taste cells, with the light cells being the most mature. Alternatively, each cell type may represent different cell lineages. The
apical ends of taste cells have microvilli that project into the taste
pore, a small opening on the dorsal surface of the tongue where
tastes cells are exposed to the oral contents. Each taste bud is
innervated by about 50 nerve fibers, and conversely, each nerve
fiber receives input from an average of five taste buds. The basal
cells arise from the epithelial cells surrounding the taste bud.
They differentiate into new taste cells, and the old cells are continuously replaced with a half-time of about 10 days. If the sensory nerve is cut, the taste buds it innervates degenerate and
eventually disappear.
In humans, the taste buds are located in the mucosa of the
epiglottis, palate, and pharynx in the walls of papillae of the
tongue (Figure 115). The fungiform papillae are rounded
structures most numerous near the tip of the tongue; the circumvallate papillae are prominent structures arranged in a V
on the back of the tongue; the foliate papillae are on the posterior edge of the tongue. Each fungiform papilla has up to five
taste buds, mostly located at the top of the papilla, while each
vallate and foliate papilla contain up to 100 taste buds, mostly
located along the sides of the papillae. The von Ebner glands
(also called gustatory glands or serous glands) secrete saliva

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Chorda tympani
nerve (VII)
Glossopharyngeal
nerve (IX)

Taste pore
Saliva
Circumvallate

Epithelial cell

Serous
gland
Taste cell

Foliate

Basal cell
Taste
bud

Fungiform

Gustatory afferent nerve

To sensory ganglion

FIGURE 115 Taste buds located in papillae of the human tongue. A) Taste buds on the anterior two-thirds of the tongue are
innervated by the chorda tympani branch of the facial nerve; those on the posterior one-third of the tongue are innervated by the lingual
branch of the glossopharyngeal nerve. B) The three major types of papillae (circumvallate, foliate, and fungiform) are located on specific parts of
the tongue. C) Taste buds are composed of basal stem cells and three types of taste cells (dark, light, and intermediate). Taste cells extend from
the base of the taste bud to the taste pore, where microvilli contact tastants dissolved in saliva and mucus. (Modified with permission from Kandel ER,
Schwartz JH, Jessell TM [editors]: Principles of Neural Science, 4th ed. New York, NY: McGraw-Hill; 2000.)

into the cleft around the circumvallate and foliate papillae.

Secretions from these glands may function to cleanse the mouth
to prepare the taste receptors for a new stimulant. Recent work
also suggests that circumvallate papilla and von Ebner glands
form a functional complex that is important in actual taste
detection because of the enzymes secreted by the gland.

TASTE PATHWAYS
The sensory nerve fibers from the taste buds on the anterior
two-thirds of the tongue travel in the chorda tympani branch
of the facial nerve, and those from the posterior third of the
tongue reach the brainstem via the glossopharyngeal nerve
(Figure 116). The fibers from areas other than the tongue
(eg, pharynx) reach the brain stem via the vagus nerve. On
each side, the myelinated but relatively slowly conducting taste
fibers in these three nerves unite in the gustatory portion of
the nucleus of the tractus solitarius (NTS) in the medulla
oblongata (Figure 116). From there, axons of second-order
neurons ascend in the ipsilateral medial lemniscus and project
directly to the ventral posteromedial nucleus of the thalamus. From the thalamus, the axons of the third-order neurons
pass to neurons in the anterior insula and the frontal operculum in the ipsilateral cerebral cortex. This region is rostral
to the face area of the postcentral gyrus, which is probably
the area that mediates conscious perception of taste and taste
discrimination.

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TASTE MODALITIES,
RECEPTORS, & TRANSDUCTION
Humans have five established basic tastes: sweet, sour,
bitter, salt, and umami. The umami taste was added to the
four classic tastes relatively recently, but it has been known
for almost 100 years. It became established as a taste modality once its receptor was identified. It is triggered particularly
by the monosodium glutamate (MSG) used so extensively
in Asian cooking. The taste is pleasant and sweet but differs
from the standard sweet taste. Although for many years it
was thought that the surface of the tongue had special areas
for each of the first four of these sensations, it is now known
that all tastants are sensed from all parts of the tongue and
adjacent structures. Afferent nerves to the NTS contain fibers
from all types of taste receptors, without any clear localization of types.
The putative receptors for the five modalities of taste are
shown diagrammatically in Figure 117. They include the two
major types of receptors: ligand-gated channels (ionotropic
receptors) and GPCRs (metabotropic receptors). Salt and
sour tastes are triggered by activation of ionotropic receptors;
sour, bitter, and umami tastes are triggered by activation of
metabotropic receptors. Many GPCRs in the human genome
are taste receptors type (T1R1, T1R2, and T1R3 families).
In some cases, these receptors couple to the heterotrimeric
G-protein, gustducin. Gustducin lowers cAMP and increases

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223

Gustatory cortex
(anterior insulafrontal operculum)

Ventral posterior
medial nucleus of
thalamus
Geniculate
ganglion

Chorda
tympani

N. VII
Tongue
Glossopharyngeal

Nucleus of
the tractus solitarius

N. IX

Petrosal
ganglion

N. X

Gustatory
areas

Nodose
ganglion

Pharynx

FIGURE 116 Diagram of taste pathways. Signals from the taste buds travel via different nerves to gustatory areas of the nucleus of the
tractus solitarius, which relays information to the thalamus; the thalamus projects to the gustatory cortex. (Modified with permission from Kandel ER,
Schwartz JH, Jessell TM [editors]: Principles of Neural Science, 4th ed. New York, NY: McGraw-Hill; 2000.)

Salt

Sour

Sweet

Bitter

Umami
(L-glutamate)

NT
NT
NT

NT

NT

NT

NT

CT

CT

CT

CT

CT

CT

CT

ENaC, others

ENaC, HCN, others

T1R2, T1R3

T2R family, others

Taste mGluR4

FIGURE 117 Signal transduction in taste receptors. Salt and sour tastes are mediated via the epithelial sodium channel (ENaC). This
receptor has two subunits ( and ), each crossing the membrane twice, resulting in intracellular N and C termini (NT, CT). Salt is sensed following
Na+ movement; sour is mediated by movement of H+. Sweet, bitter, and umami tastes are sensed via G-proteincoupled receptors that span the
membrane seven times and have varying lengths of CT and NT (represented as ribbon structures). Sweet tastes are detected by the T1R2 and
T1R3 families; bitter and umami tastes are detected by the T2R family and mGluR4, respectively.

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the formation of inositol phosphates (IP3), which can lead to

depolarization.
The salty taste is triggered by NaCl. Salt-sensitive taste
is mediated by an epithelial sodium channel (ENaC). The
entry of Na+ into the salt receptors depolarizes the membrane, generating the receptor potential. The sour taste is
triggered by protons (H+ ions). ENaCs permit the entry of
protons and may contribute to the sensation of sour taste.
The H+ ions can also bind to and block a K+-sensitive channel. The fall in K+ permeability can depolarize the membrane.
Also, a hyperpolarization-activated cyclic nucleotide-gated
cation channel (HCN) and other mechanisms may contribute to sour transduction.
Substances that taste sweet are detected by at least two
types of GPCRs, T1R2 and T1R3. Sugars taste sweet, but so do
compounds such as saccharin that have an entirely different
structure. Natural sugars such as sucrose and synthetic sweeteners may act on gustducin via different receptors. Sweetresponsive receptors act via cyclic nucleotides and inositol
phosphate metabolism.
Bitter taste is produced by a variety of unrelated compounds. Many of these are poisons, and bitter taste serves as
a warning to avoid them. Some bitter compounds bind to and
block K+-selective channels. Many GPCRs (T2R family) that
interact with gustducin are stimulated by bitter substances
such as strychnine. Some bitter compounds are membrane
permeable and their detection may not involve G-proteins;
quinine is an example.
Umami taste is due to the activation of a truncated
metabotropic glutamate receptor, mGluR4, in the taste buds.
The way activation of the receptor produces depolarization
is unsettled. Glutamate in food may also activate ionotropic
glutamate receptors to depolarize umami receptors. It is likely
that T1R1 and T1R3 receptors also detect umami taste.

TABLE 111 Some taste thresholds.

Substance

Taste

Threshold
Concentration (mol/L)

Hydrochloric acid

Sour

100

Sodium chloride

Salt

2000

Strychnine hydrochloride

Bitter

1.6

Glucose

Sweet

80,000

Sucrose

Sweet

10,000

Saccharin

Sweet

23

TASTE THRESHOLDS
& INTENSITY DISCRIMINATION
The ability of humans to discriminate differences in the intensity
of tastes, such as intensity discrimination in olfaction, is relatively
crude. A 30% change in the concentration of the substance being
tasted is necessary before an intensity difference can be detected.
Taste threshold refers to the minimum concentration at which a
substance can be perceived. The threshold concentrations of substances to which the taste buds respond vary with the particular
substance (Table 111). Bitter substances tend to have the lowest
threshold. Some toxic substances such as strychnine have a bitter
taste at very low concentrations, preventing accidental ingestion
of this chemical, which causes fatal convulsions.
A protein that binds taste-producing molecules has been
cloned. It is produced by the von Ebner gland that secretes mucus
into the cleft around circumvallate papillae (Figure 115) and
probably has a concentrating and transport function similar to
that of the OBP described for olfaction. Some common abnormalities in taste detection are described in Clinical Box 112.

CLINICAL BOX 112

Abnormalities in Taste Detection
Ageusia (absence of the sense of taste) and hypogeusia (diminished taste sensitivity) can be caused by damage to the lingual
or glossopharyngeal nerve. Neurological disorders such as vestibular schwannoma, Bell palsy, familial dysautonomia, multiple
sclerosis, certain infections (eg, primary ameboid meningoencephalopathy), and poor oral hygiene can also cause problems
with taste sensitivity. Ageusia can be an adverse side effect of various drugs, including cisplatin and captopril, or vitamin B3 or zinc
deficiencies. Aging and tobacco abuse also contribute to diminished taste. Dysgeusia or parageusia (unpleasant perception of
taste) causes a metallic, salty, foul, or rancid taste. In many cases,
dysgeusia is a temporary problem. Factors contributing to ageusia or hypogeusia can also lead to abnormal taste sensitivity. Taste
disturbances can also occur under conditions in which serotonin
(5-HT) and norepinephrine (NE) levels are altered (eg, during

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anxiety or depression). This implies that these neuromodulators

contribute to the determination of taste thresholds. Administration of a 5-HT reuptake inhibitor reduces sensitivity to sucrose
(sweet taste) and quinine (bitter taste). In contrast, administration
of an NE reuptake inhibitor reduces bitter taste and sour thresholds. About 25% of the population has a heightened sensitivity
to taste, in particular to bitterness. These individuals are called
supertasters; this may be due to the presence of an increased
number of fungiform papillae on their tongue.

THERAPEUTIC HIGHLIGHTS
Improved oral hygiene and adding zinc supplements
to ones diet can correct the inability to taste in some
individuals.

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Taste exhibits after reactions and contrast phenomena

that are similar in some ways to visual after images and contrasts. Some of these are chemical tricks, but others may be
true central phenomena. A taste-modifier protein, miraculin,
has been discovered in a plant. When applied to the tongue,
this protein makes acids taste sweet.
Animals, including humans, form particularly strong
aversions to novel foods if eating the food is followed by illness. The survival value of such aversions is apparent in terms
of avoiding poisons.

CHAPTER SUMMARY

Olfactory sensory neurons, supporting (sustentacular) cells,

and basal stem cells are located in the olfactory epithelium

within the upper portion of the nasal cavity.
The cilia located on the dendritic knob of the olfactory
sensory neuron contain odorant receptors that are coupled to
G-proteins. Axons of olfactory sensory neurons contact the
dendrites of mitral and tufted cells in the olfactory bulbs to
form olfactory glomeruli.
Information from the olfactory bulb travels via the lateral
olfactory stria directly to the olfactory cortex, including
the anterior olfactory nucleus, olfactory tubercle, piriform
cortex, amygdala, and entorhinal cortex.
Taste buds are the specialized sense organs for taste and are
composed of basal stem cells and three types of taste cells (dark,
light, and intermediate). The three types of taste cells may
represent various stages of differentiation of developing taste
cells, with the light cells being the most mature. Taste buds are
located in the mucosa of the epiglottis, palate, and pharynx and
in the walls of papillae of the tongue.
There are taste receptors for sweet, sour, bitter, salt, and
umami. Signal transduction mechanisms include passage
through ion channels, binding to and blocking ion channels,
and GPCRs requiring second messenger systems.
The afferents from taste buds in the tongue travel via
the seventh, ninth, and tenth cranial nerves to synapse
in the NTS. From there, axons ascend via the ipsilateral
medial lemniscus to the ventral posteromedial nucleus
of the thalamus, and onto the anterior insula and frontal
operculum in the ipsilateral cerebral cortex.

MULTIPLE-CHOICE QUESTIONS
For all questions, select the single best answer unless otherwise
directed.
1. A young boy was diagnosed with congenital anosmia, a rare
disorder in which an individual is born without the ability to
smell. Odorant receptors are
A. located in the olfactory bulb.
B. located on dendrites of mitral and tufted cells.
C. located on neurons that project directly to the olfactory
cortex.
D. located on neurons in the olfactory epithelium that project
to mitral cells and from there directly to the olfactory cortex.
E. located on sustentacular cells that project to the olfactory bulb.

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225

2. A 37-year-old female was diagnosed with multiple sclerosis.

One of the potential consequences of this disorder is
diminished taste sensitivity. Taste receptors
A. for sweet, sour, bitter, salt, and umami are spatially separated
on the surface of the tongue.
B. are synonymous with taste buds.
C. are a type of chemoreceptor.
D. are innervated by afferents in the facial, trigeminal, and
glossopharyngeal nerves.
E. All of the above.
3. Which of the following does not increase the ability to
discriminate many different odors?
A. Many different receptors
B. Pattern of olfactory receptors activated by a given
odorant
C. Projection of different mitral cell axons to different parts of
the brain
D. High -arrestin content in olfactory neurons
E. Sniffing
4. As a result of an automobile accident, a 10-year-old boy suffered
damage to the brain including the periamygdaloid, piriform,
and entorhinal cortices. Which of the following sensory deficits
is he most likely to experience?
A. Visual disturbance
B. Hyperosmia
C. Auditory problems
D. Taste and odor abnormalities
E. No major sensory deficits
5. Which of the following are incorrectly paired?
A. ENaC : Sour taste
B. Gustducin : Bitter taste
C. T1R3 family of GPCRs : Sweet taste
D. Heschel sulcus : Smell
E. Ebner glands : Taste acuity
6. A 9-year-old boy had frequent episodes of uncontrollable nose
bleeds. At the advice of his clinician, he underwent surgery
to correct a problem in his nasal septum. A few days after the
surgery, he told his mother he could not smell the cinnamon
rolls she was baking in the oven. Which of the following is true
about olfactory transmission?
A. An olfactory sensory neuron expresses a wide range of
odorant receptors.
B. Lateral inhibition within the olfactory glomeruli reduces
the ability to distinguish between different types of odorant
receptors.
C. Conscious discrimination of odors is dependent on the
pathway to the orbitofrontal cortex.
D. Olfaction is closely related to gustation because odorant and
gustatory receptors use the same central pathways.
E. All of the above.
7. A 31-year-old female is a smoker who has had poor oral
hygiene for most of her life. In the past few years she has
noticed a reduced sensitivity to the flavors in various foods
which she used to enjoy eating. Which of the following is not
true about gustatory sensation?
A. The sensory nerve fibers from the taste buds on the anterior
two-thirds of the tongue travel in the chorda tympani
branch of the facial nerve.

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B. The sensory nerve fibers from the taste buds on the

posterior third of the tongue travel in the petrosal branch of
the glossopharyngeal nerve.
C. The pathway from taste buds on the left side of the tongue is
transmitted ipsilaterally to the cerebral cortex.
D. Sustentacular cells in the taste buds serve as stem cells to
permit growth of new taste buds.
E. The pathway from taste receptors includes synapses in the
nucleus of the tractus solitarius in the brainstem and ventral
posterior medial nucleus in the thalamus.
8. A 20-year-old woman was diagnosed with Bell palsy (damage
to facial nerve). Which of the following symptoms is she likely
to exhibit?
A. Loss of sense of taste
B. Facial twitching
C. Droopy eyelid
D. Ipsilateral facial paralysis
E. All of the above

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