Chapter 15

15.1. Overview of the Cutaneous System

The cutaneous senses refer to everything we feel through the skin. Although touch and pain are the most
obvious feelings involving the skin, there are many others, including pressure, vibration, tickle, temperature,
and pleasure.

The Skin

M. Comèl (1953) called the skin the “monumental facade of the human body” for good reason. It is the
heaviest organ in the human body, and, if not the largest (the surface areas of the gastrointestinal tract and
of the alveoli of the lungs exceed the surface area of the skin).

In addition to its warning function, the skin also prevents body fluids from escaping and at the same time
protects us by keeping bacteria, chemical agents, and dirt from penetrating our bodies.

Skin maintains the integrity of what’s inside and protects us from what’s outside, but it also provides us with
information about the various stimuli that contact it.

The sun’s rays heat our skin, and we feel warmth; a pinprick is painful; and when someone touches us, we
experience pressure or other sensations.

On the surface of the skin is a layer of tough dead skin cells. (Try sticking a piece of cellophane tape onto your
palm and pulling it off. The material that sticks to the tape is dead skin cells.) This layer of dead cells is part of
the outer layer of skin, which is called the epidermis.

Below the epidermis is another layer, called the dermis (Figure 15.1). Within the skin are mechanoreceptors,
receptors that respond to mechanical stimulation such as pressure, stretching, and vibration.

Mechanoreceptors

Many of the tactile perceptions that we feel from stimulation of the skin can be traced to mechanoreceptors
that are located in the epidermis and the dermis.
 Two mechanoreceptors, the Merkel receptor and the Meissner corpuscle, are located close to the surface of
the skin, near the epidermis. Because they are located close to the surface, these receptors have small
receptive fields. (a cutaneous receptive field is the area of skin which, when stimulated, influences the firing
of the neuron.)

Because the nerve fiber associated with the slowly adapting Merkel receptor fires continuously, as long as the
stimulus is on, it is called a slowly adapting (SA1) fiber.

Because the nerve fiber associated with the rapidly adapting Meissner corpuscle fires only when the stimulus
is first applied and when it is removed, it is called a rapidly adapting (RA1) fiber.

The types of perception associated with the Merkel receptor/SA1 fiber are:
1. Details
2. shape, and
3. texture
with the Meissner corpuscle/RA1 fiber,
1. controlling handgrip and
2. perceiving motion across the skin.

Like the Merkel receptors, the Ruffini cylinder is a slowly adapting (SA2) fiber, which responds continuously to
stimulation. Like the Meissner corpuscle, the Pacinian corpuscle is a rapidly adapting fiber (RA2 or PC) which
responds when the stimulus is applied or removed.
Both the Ruffini cylinder and Pacinian corpuscle are located deep in the skin (Figure 15.2), so they have larger
receptive fields.

The Ruffini cylinder is associated with perceiving stretching of the skin,

the Pacinian corpuscle with sensing rapid vibrations and fine texture.
 Chapter 16

The chemical senses involve three components: taste, which occurs when molecules—often associated with
food—enter the mouth in solid or liquid form and stimulate receptors on the tongue (Figure 16.1); olfaction,
which occurs when airborne molecules enter the nose and stimulate receptor neurons in the olfactory
mucosa, located on the roof of the nasal cavity; and flavor, which is the impression we experience from the
combination of taste and olfaction.

But for taste and smell, molecules stimulate receptors that are exposed to the environment.

Because the receptors that serve taste and smell are constantly exposed not only to the chemicals they are
designed to sense but also to harmful materials such as bacteria and dirt, they undergo a cycle of birth,
development, and death over 5–7 weeks for olfactory receptors and 1–2 weeks for taste receptors. This
constant renewal of the receptors, called neurogenesis, is unique to these senses.

Because the stimuli responsible for tasting and smelling are taken into the body, these senses are often seen
as “gatekeepers” that

(1)
identify things that the body needs for survival and that should therefore be consumed and

(2)
detect things that would be bad for the body and that should therefore be rejected.

The gatekeeper function of taste and smell is aided by a large affective, or emotional, component—things
that are bad for us often taste or smell unpleasant, and things that are good for us generally taste or smell
good. In addition to creating “good” and “bad” affect, smelling an odor associated with a past place or event
can trigger memories, which in turn may create emotional reactions.

16.2. Taste Quality

Most taste researchers describe taste quality in terms of five basic taste sensations: salty, sour, sweet, bitter,
and umami (which has been described as meaty, brothy, or savory, and is often associated with the flavor-
enhancing properties of MSG, monosodium glutamate).

He found that some substances have a predominant taste quality and that other substances result in
combinations of the four taste qualities.

Connections Between Taste Quality and a Substance’s Effect

We noted that taste and olfaction can be thought of as “gatekeepers.” This is especially true for taste
because we often use taste to choose which foods to eat and which to avoid (Breslin, 2001). Taste
accomplishes its gatekeeper function by the connection between taste quality and a substance’s effect.

Sweetness is often associated with compounds that have nutritive or caloric value and that are, therefore,
important for sustaining life. Sweet compounds cause an automatic acceptance response and also trigger
anticipatory metabolic responses that prepare the gastrointestinal system for processing these substances.
Bitter compounds have the opposite effect—they trigger automatic rejection responses to help the organism
avoid harmful substances. Examples of harmful substances that taste bitter are the poisons strychnine,
arsenic, and cyanide.

Salty tastes often indicate the presence of sodium. When people are deprived of sodium or lose a great deal
of sodium through sweating, they often seek out foods that taste salty in order to replenish the salt their
body needs.

Although there are many examples of connections between a substance’s taste and its function in the body,
this connection is not perfect. People have often made the mistake of eating good-tasting poisonous
mushrooms, and there are artificial sweeteners, such as saccharine and sucralose, that have no metabolic
value. There are also bitter foods that are not dangerous and do have metabolic value. People can also learn
to modify their responses to certain tastes, as when they develop a taste for foods they may have initially
found unappealing, such as the bitter tastes in beer and coffee.

Structure

The process of tasting begins with the tongue (Figure 16.3a and Table 16.1). The surface of the
tongue contains many ridges and valleys caused by the presence of structures called papillae,
which fall into four categories:

(1)
filiform papillae, which are shaped like cones and are found over the entire surface of the
tongue, giving it its rough appearance;

(2)
fungiform papillae, which are shaped like mushrooms and are found at the tip and sides of the
tongue (see Figure 16.4);

(3)
foliate papillae, which are a series of folds along the back of the tongue on the sides; and

(4)
circumvallate papillae, which are shaped like flat mounds surrounded by a trench and are found
at the back of the tongue.
ll of the papillae except the filiform papillae contain taste buds (Figures 16.3b and 16.3c), and
the whole tongue contains about 10,000 taste buds (Bartoshuk, 1971). Because the filiform
papillae contain no taste buds, stimulation of the central part of the tongue, which contains
only these papillae, causes no taste sensations. However, stimulation of the back or perimeter
of the tongue results in a broad range of taste sensations.

Each taste bud contains 50 to 100 taste cells, which have tips that protrude into the taste pore
(Figure 16.3c). Transduction occurs when chemicals contact receptor sites located on the tips of
these taste cells (Figure 16.3d and 16.3e). Electrical signals generated in the taste cells are
transmitted from the tongue toward the brain in a number of different nerves:

(1)
the chorda tympani nerve (from taste cells on the front and sides of the tongue);

(2)
the glossopharyngeal nerve (from the back of the tongue);

(3)
the vagus nerve (from the mouth and throat); and

(4)
the superficial petrosal nerve (from the soft palete—the top of the mouth).

The fibers from the tongue, mouth, and throat make connections in the brain stem in the
nucleus of the solitary tract (Figure 16.5). From there, signals travel to the thalamus and then to
two areas in the frontal lobe that are considered to be the primary taste cortex—the insula and
the frontal operculum—which are partially hidden behind the temporal lobe

Population Coding
In Chapter 2 we distinguished between two types of coding: specificity coding, the idea that
quality is signaled by the activity in individual neurons that are tuned to respond to specific
qualities; and population coding, the idea that quality is signaled by the pattern of activity
distributed across many neurons. In that discussion, and in others throughout the book, we
have generally favored population coding. The situation for taste, however, is not clear-cut, and
there are arguments in favor of both types of coding (Frank et al., 2008).

Let’s consider some evidence for population coding. Robert Erickson (1963) conducted one of
the first experiments that demonstrated this type of coding by presenting a number of different
taste stimuli to a rat’s tongue and recording the response of the chorda tympani nerve.
Erickson called these patterns the across-fiber patterns, which is another name for population
coding. The red and green lines show that the across-fiber patterns for ammonium chloride and
potassium chloride are similar to each other but different from the pattern for sodium chloride,
indicated by the open circles.

Erickson reasoned that if the rat’s perception of taste quality depends on the across-fiber
pattern, then two substances with similar patterns should taste similar. Thus, the
electrophysiological results would predict that ammonium chloride and potassium chloride
should taste similar and that both should taste different from sodium chloride. To test this
hypothesis, Erickson shocked rats while they were drinking potassium chloride and then gave
them a choice between ammonium chloride and sodium chloride. If potassium chloride and
ammonium chloride taste similar, the rats should avoid the ammonium chloride when given a
choice. This is exactly what they did. And when the rats were shocked for drinking ammonium
chloride, they subsequently avoided the potassium chloride, as predicted by the
electrophysiological results.

But what about the perception of taste in humans? When Susan Schiffman and Robert Erickson
(1971) asked humans to make similarity judgments between a number of different solutions,
they found that substances that were perceived to be similar were related to patterns of firing
for these same substances in the rat. Solutions judged more similar psychophysically had similar
patterns of firing, as population coding would predict.

Specificity Coding

It is important to note that in all these experiments, adding or eliminating bitter receptors had
no effect on neural firing or behavior to sweet, sour, salty, or umami stimuli. Other research
using similar techniques has identified receptors for sugar and umami (Zhao et al., 2003).

The results of these experiments in which adding a receptor makes an animal sensitive to a
specific quality and eliminating a receptor makes an animal insensitive to a specific quality have
been cited as support for specificity coding—that there are receptors that are specifically tuned
to sweet, bitter, and umami tastes. However, not all researchers agree that the picture is so
clear-cut. For example, Eugene Delay and coworkers (2006) showed that with different
behavioral tests, mice that appeared to have been made insensitive to sugar by eliminating a
“sweet” receptor can actually still show a preference for sugar. Based on this result, Delay
suggests that perhaps there are a number of different receptors that respond to specific
substances like sugar.

Another line of evidence for specificity coding in taste has come from research on how single
neurons respond to taste stimuli. Recordings from neurons at the beginning of the taste
systems of animals, ranging from rats to monkeys, have revealed neurons that are specialized
to respond to specific stimuli, as well as neurons that respond to a number of different types of
stimuli (Lundy & Contreras, 1999; Sato et al., 1994; Spector & Travers, 2005).

Another finding in line with specificity theory is the effect of presenting a substance called
amiloride, which blocks the flow of sodium into taste receptors. Applying amiloride to the
tongue causes a decrease in the responding of neurons in the rat’s brainstem (nucleus of the
solitary tract) that respond best to salt (Figure 16.9a) but has little effect on neurons that
respond best to a combination of salty and bitter tastes (Figure 16.9b; Scott & Giza, 1990). Thus,
eliminating the flow of sodium across the membrane selectively eliminates responding of salt-
best neurons but does not affect the response of neurons that respond best to other tastes. As
it turns out, the sodium channel that is blocked by amiloride is important for determining
saltiness in rats and other animals, but not in humans. More recent research has identified
another channel that serves the salty taste in humans

argue for population coding based on the finding that at more central locations in the taste
system, neurons are tuned broadly, with many neurons responding to more than one taste
quality.

point out that just because there are neurons that respond best to one compound like salty or
sour, this doesn’t mean that these tastes are signaled by just one type of neuron. They illustrate
this by drawing an analogy between taste perception and the mechanism for color vision. Even
though presenting a long-wavelength light that appears red may cause the highest activation in
the long-wavelength cone pigment (see Figure 9.15), our perception of red still depends on the
combined response of both the long- and medium-wavelength pigments. Similarly, salt stimuli
may cause high firing in neurons that respond best to salt, but other neurons are probably also
involved in creating saltiness.

One suggestion is that basic taste qualities might be determined by a specific code, but
population coding could determine subtle differences between tastes within a category
(Pfaffmann, 1974; Scott & Plata-Salaman, 1991). This would help explain why not all substances
in a particular category have the same taste. For example, the taste of all sweet substances is
not identical (Lawless, 2001).

Because of arguments such as this, some researchers believe that even though there is good
evidence for specific taste receptors, population coding is involved in determining taste as well,
especially at higher levels of the system.
16.4. Individual Differences in Taste

The “taste worlds” of humans and animals are not necessarily the same. For example, domestic
cats, unlike most mammals, don’t prefer the sweetness of sugar, even though they display
human-like taste behavior to other compounds, such as avoiding compounds that taste bitter
or very sour to humans. Genetic research has shown that this “sweet blindness” occurs because
cats lack a functional gene for formation of a sweet receptor and so, lacking a sweet receptor,
have no mechanism for detecting sweetness (Li et al., 2005).

This interesting fact about cats has something to tell us about human taste perception, because
it turns out that there are genetic differences that affect people’s ability to sense the taste of
certain substances. One of the best-documented effects involves people’s ability to taste the
bitter substance phenylthiocarbamide (PTC), which we discussed earlier in connection with
Mueller’s experiments on specificity coding. The discovery of the PTC effect has been described
as follows:

People who can taste PTC are described as tasters, and those who cannot are called nontasters.

One explanation for these differences is that people who can taste PROP have higher densities
of taste buds than those who can’t taste it

A factor that determines individual differences in taste, in addition to receptor density, is the
presence of specialized receptors. Advances in genetic techniques have made it possible to
determine the locations and identities of genes on human chromosomes that are associated
with taste and smell receptors. These studies have shown that PROP and PTC tasters have
specialized receptors that are absent in nontasters

f PROP tasters also perceived other compounds as being more bitter than nontasters, then
certain foods might taste more bitter to the tasters. The evidence on this question, however,
has been mixed. Some studies have reported differences between how tasters and nontasters
rate the bitterness of other compounds (Bartoshuk, 1979; Hall et al., 1975), and others have not
observed this difference (Delwiche et al., 2001b). However, it does appear that people who are
especially sensitive to PROP, called supertasters, may actually be more sensitive to most bitter
substances, as if the amplification in the bitter taste system is turned up for all bitter
compounds (Delwiche et al., 2001a).

It may reflect not a difference in preference (you like sweet things more than John does) but a
difference in perception (you perceive sweet tastes as more intense than John does), which
could be caused by differences in the types and numbers of taste receptors on the tongue or
other differences in your taste systems.

16.5. The Importance of Olfaction

At the beginning of the chapter we noted that taste and olfaction have often been described as
being less important than vision and hearing. The importance of olfaction has also been
minimized in many textbooks, which describe human olfaction as being microsmatic (having a
poor sense of smell that is not crucial to survival), while describing olfaction in other animals,
and especially dogs, as macrosmatic—having a well-developed sense of smell (McGann, 2017).

But recent measurements of the sensitivity of humans and animals to different odors indicates
that humans are more sensitive to many odors than a wide range of animals, including mice,
monkeys, rabbits, and seals. And although dogs are far more sensitive than humans to some
odors, human’s sensitivity equals dog’s for others (Laska, 2017).

16.6. Olfactory Abilities

Detecting Odors

Our sense of smell enables us to detect extremely low concentrations of some odorants. The
detection threshold for odors is the lowest concentration at which an odorant can be detected.
One method for measuring detection thresholds is the forced-choice method, in which
participants are presented with blocks of two trials—one trial contains a weak odorant and the
other, no odorant. The participant’s task is to indicate which trial has a stronger smell. The
threshold is determined by measuring the concentration that results in a correct response on
75 percent of the trials (50 percent would be chance performance).

It is notable that there is a very large range of thresholds

Identifying Odors

One of the more intriguing facts about odors is that even though humans can discriminate
millions or perhaps trillions of different odors, they often find it difficult to accurately identify
specific odors. For example, when people are presented with the odors of familiar substances
such as mint, bananas, and motor oil, they can easily tell the difference between them.
However, when they are asked to identify the substance associated with the odor, they are
successful less than half the time (Desor & Beauchamp, 1974; Engen & Pfaffmann, 1960).
However, when people are trained in identifying odors by being told the names of substances
when they first smell them and then being reminded of the correct names if they fail to name
them correctly on subsequent presentations, they can eventually identify 98 percent of the
substances

one of the amazing things about odor identification is that knowing the correct label for the
odor actually seems to transform our perception into that odor. (club taste thingy)

Thus, when we have trouble identifying odors, this trouble may occur not because of a
deficiency in our olfactory system, but from an inability to retrieve the odor’s name from our
memory
Individual Differences in Olfaction

We noted earlier that there are people with anosmia who have lost their sense of smell (p.
389). There are also genetic conditions which cause selective losses of some smells. For
example, a section of the human chromosome is associated with receptors that are sensitive to
the chemical β-ionone, which is often added to foods and beverages to add a pleasant floral
note. Individuals sensitive to β-ionone describe paraffin with low concentrations of β-ionone
added as “fragrant” or “floral,” whereas individuals with less sensitivity to β-ionone describe
the same stimulus as “sour,” “pungent,” or “acid” (Jaeger et al., 2013). Genetically caused
variation in sensitivity occurs for many other chemicals, as well, leading to the idea that
everyone experiences his or her own unique “flavor world”

Loss of Smell in COVID-19 and Alzheimer’s Disease

One explanation that has been proposed is that COVID molecules attach to an enzyme called
ACE2 that is found in the intestines, lungs, arteries, and heart, and which has recently been
found in the nose. Figure 16.11 shows that ACE2 is found on the surface of sustentacular cells,
which provide metabolic and structural support to the olfactory sensory neurons (Bilinska et al.,
2020). It has been proposed, therefore, that COVID-19 causes loss of smell not by directly
attacking sensory neurons but by affecting their supporting cells. Exactly how this causes a loss
of smell is still being investigated.

Loss of smell is also associated with Alzheimer’s disease (AD), a serious loss of memory and
other cognitive functions that is often preceded by mild cognitive impairment (MCI), which has
affected 50 million people worldwide (Bathini et al., 2019). But an important difference
between the olfactory losses associated with AD and COVID-19 is that in AD the loss of olfaction
begins occurring decades before the occurrence of clinical symptoms such as memory loss and
difficulties in reasoning (Bathini et al., 2019; Devanand et al., 2015). This is shown in Figure
16.12, which tracks the progression of the loss of cognition that is the primary symptom of AD
(purple curve) and the progression of “biomarkers” associated with AD (Bathini et al., 2019).
Notice that the curves for the biomarkers start rising much earlier than the curve for the loss of
cognition. The fastest biomarker curve is for Amyloid B (red curve), which is associated with
formation of plaques in the brain, and the next-fastest curve is for loss of olfaction (dashed
curve).

bnormal olfactory functioning rises very rapidly during the preclinical phase (yellow shading),
and is very high before symptoms of MCI and Alzheimer’s begin appearing. This property has
led to the proposal that measuring olfactory function is a way to achieve early diagnosis of
Alzheimer’s, which, in turn, would make it possible to start treatment earlier. (Although there is
no cure for AD, treatments are being developed that may slow the development of clinical
symptoms.)

Another difference between olfactory loss in AD and in COVID-19 is that the olfactory system
may suffer from more widespread attack in AD. There is evidence that AD attacks not only the
olfactory bulb, but more central structures, as well. The key conclusion is that the olfactory
system appears to be much more sensitive than the visual system or auditory system to neural
dysfunction. Thus, although some visual loss precedes AD symptoms, the loss of olfactory
function is the key sensory biomarker for predicting development of AD. A related finding is
that loss of olfaction is also associated with a higher risk of death. Jayant Pinto and coworkers
(2014) found that in a group of older adults (57–87 years old), who were representative of the
general U.S. population, people with anosmia (loss of smell) were three times more likely to die
within five years than people with normal smell.

16.7. Analyzing Odorants: The Mucosa and Olfactory Bulb

We have, so far, been describing the functions of olfaction and the experiences that occur when
olfactory stimuli, molecules in the air, enter the nose. We now consider the question of how
the olfactory system knows what molecules are entering the nose.

The Puzzle of Olfactory Quality

One reason for the difficulty is that we lack a specific language for odor quality. For example,
when people smell the chemical α-ionone, they usually say that it smells like violets. This
description, it turns out, is fairly accurate, but if you compare α-ionone to real violets, they
smell different. The perfume industry’s solution is to use names such as “woody violet” and
“sweet violet” to distinguish between different violet smells, but this hardly solves the problem
we face in trying to determine how olfaction works.

Another difficulty in relating odors to molecular properties is that some molecules that have
similar structures can smell different (Figure 16.13a), and molecules that have very different
structures can smell similar (Figure 16.13b). But things really become challenging when we
consider the kinds of odors we routinely encounter in the environment, which consist of
mixtures of many chemicals. Consider, for example, that when you walk into the kitchen and
smell freshly brewed coffee, the coffee aroma is created by more than 100 different molecules.
Although individual molecules may have their own odors, we don’t perceive the odors of
individual molecules; we perceive “coffee.”

Sources of odors such as coffee, bacon, and orange juice, as well as nonfood sources such as
rose, dog, and car exhaust, are called odor objects. Our goal, therefore, is to explain not just
how we smell different odor qualities, but how we identify different odor objects.

Perceiving odor objects involves olfactory processing that occurs in two stages. The first stage,
which takes place at the beginning of the olfactory system in the olfactory mucosa and
olfactory bulb, involves analyzing. In this stage, the olfactory system analyzes the different
chemical components of odors and transforms these components into neural activity at specific
places in the olfactory bulb (Figure 16.15). The second stage, which takes place in the olfactory
cortex and beyond, involves synthesizing. In this stage, the olfactory system synthesizes the
information about chemical components received from the olfactory bulb into representations
of odor objects. As we will see, it has been proposed that this synthesis stage involves learning
and memory.
The Olfactory Mucosa
The olfactory mucosa is a dime-sized region located on the roof of the nasal cavity just below
the olfactory bulb (Figure 16.15a). Odorant molecules are carried into the nose in an air stream
(blue arrows), which brings these molecules into contact with the mucosa. Figure 16.15b shows
the olfactory receptor neurons (ORNs) that are located in the mucosa (colored parts) and the
supporting cells (tan area).

Just as the rod and cone receptors in the retina contain visual pigment molecules that are
sensitive to light, the olfactory receptor neurons in the mucosa are dotted with molecules
called olfactory receptors that are sensitive to chemical odorants (Figure 16.15c). One parallel
between visual pigments and olfactory receptors is that they are both sensitive to a specific
range of stimuli. Each type of visual pigment is sensitive to a band of wavelengths in a particular
region of the visible spectrum (see Figure 9.13), and each type of olfactory receptor is sensitive
to a narrow range of odorants.

Just as the rod and cone receptors in the retina contain visual pigment molecules that are
sensitive to light, the olfactory receptor neurons in the mucosa are dotted with molecules
called olfactory receptors that are sensitive to chemical odorants (Figure 16.15c). One parallel
between visual pigments and olfactory receptors is that they are both sensitive to a specific
range of stimuli. Each type of visual pigment is sensitive to a band of wavelengths in a particular
region of the visible spectrum (see Figure 9.13), and each type of olfactory receptor is sensitive
to a narrow range of odorants.

However, an important difference between the visual system and the olfactory system is that
while there are only four different types of visual pigments (one rod pigment and three cone
pigments), there are about 400 different types of olfactory receptors, each sensitive to a
particular group of odorants.

The large number of olfactory receptor types increases the challenges in understanding how
olfaction works. One thing that makes things slightly simpler is another parallel with vision: Just
as a particular rod or cone receptor contains only one type of visual pigment, a particular
olfactory receptor neuron (ORN) contains only one type of olfactory receptor.

How Olfactory Receptor Neurons Respond to Odorants

The first step in understanding how we perceive different odorants is to ask how this array of
millions of ORNs that blanket the olfactory mucosa respond to different odorants. One way this
question has been answered is by using a technique called calcium imaging.

The pattern of activation for each odorant, which is indicated by reading across each row, is
called the odorant’s recognition profile.

From these profiles, we can see that each odorant causes a different pattern of firing across
ORNs. Also, odorants that have similar structures (shown on the right in Figure 16.17), such as
octanoic acid and nonanoic acid, often have similar profiles. We can also see, however, that this
doesn’t always occur (compare the patterns for bromohexanoic acid and bromooctanoic acid,
which also have similar structures).

Remember that one of the puzzling facts about odor perception is that some molecules have
similar structures but smell different (Figure 16.13a). When Malnic compared such molecules,
she found that these molecules had different recognition profiles. For example, octanoic acid
and octanol differ only by one oxygen molecule, but the smell of octanol is described as
“sweet,” “rose,” and “fresh,” whereas the smell of octanoic acid is described as “rancid,”
“sour,” and “repulsive.” This difference in perception is reflected in their different profiles.
Although we still can’t predict which smells result from specific patterns of response, we do
know that when two odorants smell different, they usually have different profiles.

The situation for odors is similar—each odorant is coded by a different pattern of firing of
ORNs, and a particular ORN responds to many odorants.

The Search for Order in the Olfactory Bulb

Activation of receptors in the mucosa causes electrical signals in the ORNs that are distributed
across the mucosa. These ORNs send signals to structures called glomeruli in the olfactory bulb.
Figure 16.16b illustrates a basic principle of the relationship between ORNs and glomeruli: All of
the ORNs of a particular type send their signals to just one or two glomeruli, so each glomerulus
collects information about the firing of a particular type of ORN.

This targeting of specific areas of the olfactory bulb by certain receptors creates different
patterns of olfactory bulb activation for different odorants.

The different patterns for different odorants create a map of odorants in the olfactory bulb that
it is based on molecular features of odorants such as carbon chain length or functional groups.
These maps have been called chemotopic maps (Johnson & Leon, 2007; Johnson et al., 2010;
Murthy, 2011), odor maps (Restrepo et al., 2009; Soucy et al., 2009; Uchida et al., 2000), and
odotoptic maps (Nikonov et al., 2005).

The different patterns for different odorants create a map of odorants in the olfactory bulb that
it is based on molecular features of odorants such as carbon chain length or functional groups.
These maps have been called chemotopic maps (Johnson & Leon, 2007; Johnson et al., 2010;
Murthy, 2011), odor maps (Restrepo et al., 2009; Soucy et al., 2009; Uchida et al., 2000), and
odotoptic maps (Nikonov et al., 2005).

16.8. Representing Odors in the Cortex

To begin our discussion of how odors are represented in the cortex, let’s look at where signals
are transmitted when they leave the olfactory bulb. Figure 16.20a shows the location of the two
main olfactory areas:
(1)
the piriform cortex (PC), which is the primary olfactory area, and

(2)
the orbitofrontal cortex, which is the secondary olfactory area.

Figure 16.20b shows the olfactory system as a flow diagram and adds the amygdala, which is
involved in determining emotional reactions not only to smell but also to faces and pain. We
begin by considering the piriform cortex.

How Odorants Are Represented in the Piriform Cortex

Odors that smell different cause different patterns of firing of olfactory receptors (Figure 16.17).
Moving to the olfactory bulb, different chemicals cause activity in specific areas, which has led
to the proposal of odotopic maps

But when we move up to the piriform cortex (PC), something surprising happens: The map
vanishes! Odorants that caused activity in specific locations in the olfactory bulb now cause
widespread activity in the PC, and there is overlap between the activity caused by different
odorants.

These results show that the orderly activation pattern in the olfactory bulb no longer exists in
the piriform cortex. This occurs because the projection from the olfactory bulb is scattered, so
activity associated with a single chemical is spread out over a large area. Things become even
more interesting when we ask what the activation pattern might look like for an odor object
such as coffee.

How Odor Objects Are Represented in the Piriform Cortex

e can appreciate how complicated things become for odor objects by imagining what the
pattern of activation would be for coffee, which contains a hundred different chemical
components. Not only will the pattern be very complicated, but if you are smelling a particular
odor for the first time, this raises the question of how the olfactory system is able to determine
the identity of this “mystery odor” based on the information in this first-time response. Some
researchers have answered this question by drawing a parallel between recognizing odors and
experiencing memories.

Figure 16.23 indicates what happens when a memory is formed. When a person witnesses an
event, a number of neurons are activated (Figure 16.23a). At this point, the memory for the
event isn’t completely formed in the brain; it is fragile and can be easily forgotten or can be
disrupted by trauma, such as a blow to the head. But connections begin forming between the
neurons that were activated by the event (Figure 16.23b), and after these connections are
formed (Figure 16.23c), the memory is stronger and more resistant to disruption. Formation of
stable memories thus involves a process in which linkages are formed between a number of
neurons.

Applying this idea to odor perception, it has been proposed that formation of odor objects
involves learning, which links together the scattered activations that occur for a particular
object. We can see how this works by imagining that you are smelling the odor of a flower for
the first time. The odor of this flower, just like the odors of coffee and other substances, is
created by a large number of chemical compounds (Figure 16.24a). These chemical components
first activate the olfactory receptors in the mucosa and then create a pattern of activation on
the olfactory bulb that is shaped by the chemotopic map. This pattern occurs any time the
flower’s odor is presented (Figure 16.24b). From the research described above, we know that
signals from the olfactory bulb are transformed into a scattered pattern of activation in the
piriform cortex (Figure 16.24c).

Because this is the first time you have ever experienced the flower’s odor, the activated
neurons aren’t associated with each other. This is like the neurons that represent a new
memory, which aren’t yet linked (see Figure 16.23a). At this point you are likely to have trouble
identifying the odor and might confuse it with other odors. But after a number of exposures to
the flower, which cause the same activation pattern to occur over and over, neural connections
form, and the neurons become associated with each other (Figure 16.24d). Once this occurs, a
pattern of activation has been created that represents the flower’s odor. Thus, just as a stable
memory becomes established when neurons become linked, odor objects become formed
when experience with an odor causes neurons in the piriform cortex to become linked.

Wilson concluded from these results that, given enough time, neurons in the piriform cortex
can learn to discriminate between different odors, and that this learning may be involved in our
ability to tell the difference between different odors in the environment. Numerous other
experiments support the idea that a mechanism involving experience and learning is involved in
associating patterns of piriform cortex firing with specific odor objects

How Odors Trigger Memories

called the Proust effect. This passage captures some characteristics of Proustian memories:

(1)
Memories were realized not by seeing the cookie but by tasting it;

(2)
the memory was vivid and transported Proust back to a number of places from his past; and

(3)
the memory was from Proust’s early childhood.
Modern researchers call these Proustian memories odor-evoked autobiographical memories
(OEAMs), because they are elicited by odors and are memories about events from a person’s
life story. But OEAMs aren’t simply a literary observation.

The result was that participants who smelled the odor rated their memories as more emotional
than participants who saw the picture. They also had a stronger feeling than the visual group of
“being brought back” to the time the memory occurred

Memories elicited by odors were most likely to be for events that occurred in the first decade
of life, whereas memories elicited by words were more likely to be for events from the second
decade of life. The participants in this experiment also described their odor-evoked memories
as being associated with strong emotions and feelings of being brought back in time.

A clue to the answer is that the amygdala, which is involved in creating emotions and emotional
memories, is only two synapses from the olfactory nerve, and the hippocampus, which is
involved in storing and retrieving memories, is only three synapses away

Chemicals in food or drink cause taste when they activate taste receptors on the tongue. But in
addition, food and drink release volatile chemicals that reach the olfactory mucosa by following
the retronasal route, from the mouth through the nasal pharynx, the passage that connects the
oral and nasal cavities (Figure 16.1). Although pinching the nostrils shut does not close the nasal
pharynx, it prevents vapors from reaching the olfactory receptors by eliminating the circulation
of air through this channel (Murphy & Cain, 1980). The same thing happens when you have a
cold—less airflow means the flavor of foods will be greatly reduced.

One reason this localization of flavor occurs is because food and drink stimulate tactile
receptors in the mouth, which creates oral capture, in which the sensations we experience from
both olfactory and taste receptors are referred to the mouth

Although taste and olfactory stimuli occur in close proximity in the mouth and nose, our
perceptual experience of their combination is created when they interact in the cortex.

In addition, vision and touch contribute to flavor by sending signals to the amygdala (vision),
structures in the taste pathway (touch), and the orbitofrontal cortex (vision and touch).

ll of these interactions among taste, olfaction, vision, and touch underscore the multimodal
nature of our experience of flavor. Flavor includes not only what we typically call “taste,” but
also perceptions such as the texture and temperature of food (Verhagen et al., 2004), the color
of food (Spence, 2015; Spence et al., 2010), and the sounds of “noisy” foods such as potato
chips and carrots that crunch when we eat them

Because of this convergence of neurons from different senses, the orbitofrontal cortex contains
many bimodal neurons, neurons that respond to more than one sense.
An important property of these bimodal neurons is that they often respond to similar qualities.
Thus, a neuron that responds to the taste of sweet fruits would also respond to the smell of
these fruits.

Because of these properties, it has been suggested that the orbitofrontal cortex is a cortical
center for detecting flavor and for the perceptual representation of foods (Rolls & Baylis, 1994;
Rolls et al., 2010). Other research has shown that the insula, the primary taste cortex, is also
involved in the perception of flavor (de Araujo et al., 2012; Veldhuizen et al., 2010).

ith the $90 wine causing a much large response (Figure 16.28b).

This larger effect on the odor associated with the food eaten to satiety, called sensory-specific
satiety, also occurred in the response of the orbitofrontal cortex. The orbitofrontal cortex
response decreased for the banana odor but remained the same for the vanilla odor (Figure
16.29b). Similar effects also occurred in the amygdala and insula for some (but not all)
participants.

The orbitofrontal cortex is involved in determining the reward value of foods. Food is more
rewarding when you are hungry and becomes less rewarding as food is consumed, until
eventually—at satiety—the reward is gone and eating stops. These changes in the reward value
of flavors are important because just as taste and olfaction are important for warning of
danger, they are also important for regulating food intake

What we’ve learned by considering each of the stages of the systems for taste, olfaction, and
flavor is that the purpose of the chemical senses extends beyond simply creating experiences of
taste, smell, and flavor. Their purpose is to help guide behavior—avoiding potentially harmful
substances, seeking out nutrients, and helping control the amount of food consumed. In fact,
even neurons in the olfactory bulb are sensitive to signals the body creates about hunger and
satiety. Thus they respond to food odors in the context of signals from the body about how
hungry you are.