276 Chapter 10
impulses to the brain, where they are interpreted as the corre-
sponding taste perception.
Although all sweet and bitter taste receptors act via
G- proteins, the second-messenger systems activated by the
G-proteins depend on the molecule tasted. In the case of the
sweet taste of sugars, for example, the G-proteins activate
adenylate cyclase, producing cyclic AMP (cAMP; see chap-
ter 7). The cAMP, in turn, produces depolarization by closing
K^1 channels that were previously open. On the other hand, the
sweet taste of the amino acids phenylalanine and tryptophan,
as well as of the artificial sweeteners saccharin and cyclamate,
may enlist different second-messenger systems. These involve
the activation of a membrane enzyme that produces the sec-
ond messengers inositol triphosphate (IP 3 ) and diacylglycerol
(DAG). These second-messenger systems are described in
chapter 11, section 11.2.Smell
The receptors responsible for olfaction, the sense of smell, are
located in the olfactory epithelium. The olfactory apparatus
consists of receptor cells (which are bipolar neurons), sup-
porting (sustentacular) cells, and basal stem cells. The stem
cells generate new receptor cells every one to two months to
replace the neurons damaged by exposure to the environment.
The supporting cells are epithelial cells rich in enzymes that
oxidize hydrophobic volatile odorants, thereby making these
molecules less lipid-soluble and thus less able to penetrate
membranes and enter the brain.
Each bipolar sensory neuron has one dendrite that projects
into the nasal cavity, where it terminates in a knob containing
cilia ( figs. 10.9 and 10.10 ). It is the plasma membrane cover-
ing the cilia that contains the receptor proteins that bind to
odorant molecules. Although humans have about a thousand
genes coding for olfactory receptors, most of these have accu-
mulated mutations that prevent them from being expressed
(they are “pseudogenes”), leaving an estimated 380 genes that
code for 380 different olfactory receptor proteins. Through
work that was awarded the Nobel Prize in Physiology or
Medicine in 2004, scientists discovered that each olfactory
sensory neuron expresses only one gene that produces only
one type of these receptor proteins. The axon of each olfac-
tory neuron thereby conveys information relating only to the
specific odorant molecule that stimulated that neuron.
The olfactory receptors are G-protein-coupled receptors.
This means that before the odorant molecule binds to its recep-
tor, the receptor is associated with the three G-protein subunits
( a , b , and g ). When an odorant molecule binds to its recep-
tor, these subunits dissociate, move in the plasma membrane
to adenylate cyclase, and activate this enzyme. Adenylate (or
adenyl) cyclase catalyzes the conversion of ATP into cyclic
AMP (cAMP) and PP i (pyrophosphate). The cAMP serves as
a second messenger, opening ion channels that allow inward
diffusion of Na^1 and Ca^2 1 ( fig. 10.11 ). This produces a graded
depolarization, the receptor potential, which then stimulates
the production of action potentials.and texture of food, which stimulate receptors around the taste
buds in the tongue.
The salty taste of food is due to the presence of sodium
ions (Na^1 ), or some other cations, which activate specific
receptor cells for the salty taste. Different substances taste
salty to the degree that they activate these particular receptor
cells. The Na^1 passes into the sensitive receptor cells through
channels in the apical membranes. This depolarizes the cells,
causing them to release their transmitter. The anion associated
with the Na^1 , however, modifies the perceived saltiness to a
surprising degree: NaCl tastes much saltier than other sodium
salts (such as sodium acetate). Salt is appetitive (attractive) at
low concentrations but becomes aversive at higher salt con-
centrations. A recent report suggests that the aversive effect of
high salt concentrations is produced by activation of the bitter
and sour taste pathways.
Sour taste, like salty taste, is produced by ion move-
ment through membrane channels. Sour taste, however, is
due to the presence of hydrogen ions (H^1 ); all acids there-
fore taste sour, and the degree of sourness corresponds to
the fall in pH within the taste cells. In contrast to the salty
and sour tastes, the sweet and bitter tastes are produced
by interaction of taste molecules with specific membrane
receptor proteins.
The remaining three taste modalities—sweet, bitter, and
umami—all involve interactions of the taste molecules with
membrane receptors coupled to G-proteins ( fig. 10.8 ). The
ability of sweet receptors to respond to a wide variety of
organic molecules is apparently due to the presence of multiple
ligand binding sites in the receptor proteins. Most organic mol-
ecules, but particularly sugars, taste sweet to varying degrees
when they bind to the G-protein-coupled receptors on the
taste cells “tuned” to detect a sweet taste. Umami, the most
recently discovered taste, evokes a savory, “meaty” sensation
in response to proteins, and (along with the sweet taste) is an
attractive taste modality. In humans, the G-protein-coupled
umami receptors are activated only by binding of the amino
acids L-glutamate and L-aspartate. Because any protein will
have these amino acids in it, this is apparently sufficient to
impart the umami taste modality.
Whereas the sweet and umami tastes are appetitive, the
bitter taste is aversive and serves to warn against toxins.
Accordingly, these receptors are more sensitive to low concen-
trations of their ligands than are the sweet and umami recep-
tors. Also, bitter receptors are able to detect a wide variety
of toxic chemicals but do not appear to distinguish between
them. Bitter taste is apparently indistinguishable if evoked by
quinine or seemingly unrelated molecules that stimulate the
bitter receptors. It should be noted that, although the bitter
taste is generally associated with toxic molecules, not all tox-
ins taste bitter.
The G-proteins involved in taste have been termed
gustducins. Dissociation of the gustducin G-protein subunit
activates second-messenger systems, leading to depolarization
of the receptor cell ( fig. 10.8 ). The stimulated receptor cell,
in turn, activates an associated sensory neuron that transmits