Lippincott Illustrated Reviews: Physiology (Lippincott Illustrated Reviews Series)

Taste and Smell

10

I. OVERVIEW

The gustatory and olfactory systems are probably the oldest of the senses in evolutionary terms. Both systems allow us to detect chemicals in the external environment and, thus, are usually grouped together. In practice, however, they represent two very different sensory modalities that complement but cannot replace each other. Taste cells are modified epithelial cells, whereas olfactory receptors are neurons. Taste allows us to differentiate between very basic flavors, such as sweet versus salty, or savory versus sour. Taste is closely linked with appetite and cravings, such as a need to ingest salt (NaCl) or something sweet, and it is also protective. Bitter taste often helps us avoid ingesting toxins, whereas the taste of acid (sour) often indicates food decay. Olfaction allows us to detect and identify thousands of unique chemicals, including pheromones.

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II. TASTE

There are five basic tastes: saltysweetumamibitter, and sour (Table 10.1). Umami (“good taste” in Japanese) is epitomized by the taste of monosodium glutamate (MSG), which imparts a savory, meaty flavor to food. The taste of fat constitutes a sixth basic taste, but the transduction mechanisms are not fully delineated. The chemical sensations that mimic hot (e.g., the burning sensation associated with chili peppers) and cold (e.g., menthol) are not tastes but rather are mediated by somatosensory pathways located in the oral cavity or nasal passage (see 16·VII·B).

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Figure 10.1

Taste bud organization.

A. Taste buds

Taste receptor cells are usually clustered in taste buds, which are distributed throughout the oral cavity. Lingual taste buds are organized like garlic bulbs (Figure 10.1), each containing ~100 elongated neuroepithelial cell “cloves.” Adjacent cells are connected apically by tight junctions. Some cells extend microvilli into a taste bud's small central pore, which provides a way for oral fluids (saliva) and their dissolved tastants to enter the taste bud and be sensed. Taste buds contain several different cell types: Type I, II, and III cells are all taste receptors.

B. Type I cells

Type I receptors are nonexcitable cells that transduce salty taste, epitomized by the taste of NaCl (table salt) and, more specifically, Na+. Type I cells have glia-like properties (see 5·V) and transduce Na+sensation using an epithelial Na+ channel (ENaC).

1. Glia-like function: Type I cells extend membrane processes that surround other cells within the taste bud and may help regulate extracellular K+ concentrations during excitation. Type I cells also help terminate signaling by hydrolyzing neurotransmitter soon after release (see Section E below).

2. Transduction: Type I cells sense salt using ENaC. ENaC is always open, so when salty foods are ingested, Na+ ions flood into the cells, and the receptor depolarizes (Figure 10.2). Receptor potential amplitude is graded with Na+ concentration, but the downstream consequences of this receptor potential are still being investigated.

C. Type II cells

Type II cells are excitable sensory receptors. Their membranes contain specific G protein–coupled receptors (GPCRs) that mediate sweet, umami, and bitter tastes, but they do not respond to salty or sour tastants. Individual type II cells are tastant specific.

1. Tastants: The three tastant classes detected by type II cells (sweet, umami, and bitter) are perceived as either being pleasant and signaling the presence of food or noxious and indicative of a toxin.

a. Sweet: Sweet tastes are associated with mono- and disaccharides, such as glucose and sucrose. Sugars are a primary energy source, and, therefore, the ability to recognize their presence in food has clear evolutionary advantages. Sugars are sensed by a single GPCR with a T1R2–T1R3 heterodimeric composition.

The extracellular domain of the sweet taste receptor is large and shaped like a Venus flytrap. The domain contains binding sites for sugars, but it also recognizes certain proteins as sweet (e.g., monellin). This feature has facilitated the development of a wide range of synthetic peptide sweeteners, including aspartame.

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Figure 10.2

Type I receptor cell taste transduction. ENaC = epithelial Na+ channel.

b. Umami: The savory taste is elicited by glutamate, which is released from meat during protein hydrolysis. Some nucleotides (inosine monophosphate and guanosine monophosphate) also produce umami taste. Glutamate elicits at least some of its effects by binding to a T1R1–T1R3 heterodimeric GPCR.

c. Bitter: Many plants, fungi, and some animals produce toxins as a natural defense mechanism. Evolution has helped guide our choice of food by associating many such poisons with a bitter taste. Most bitter tastants are detected by GPCRs. Toxins are such a diverse group that recognizing them as such requires specific receptor proteins. Taste cells that sense bitter stimuli express subsets of >20 GPCR T2R variants. Some are highly tastant specific, whereas others have broad specificity.

Quinine is a bitter-tasting toxin with antimalarial properties extracted from cinchona tree bark. It blocks most classes of K+ channel and causes nonspecific membrane depolarization.

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Figure 10.3

Type II receptor cell taste transduction. ATP = adenosine triphosphate; GPCRs = G protein–coupled receptors; PLC = phospholipase C; TRPM5 = transient receptor potential M5 channel.

2. Transduction: Tastant binding to its GPCR activates gustducin, a G protein that signals receptor occupancy through adenosine triphosphate (ATP) release into the taste bud interstitium (Figure 10.3).

a. Activation: The gustducin Gβγ unit activates phospholipase C (PLC) and initiates inositol trisphosphate–induced Ca2+ release from intracellular stores. Ca2+ then activates influx of Ca2+ and other cations via TRPM5 (a transient receptor potential channel; see 2·VI·D), and the receptor cell depolarizes. The gustducin Gα subunit modifies intracellular cyclic adenosine monophosphate (cAMP) levels through modulation of adenylyl cyclase, but the consequences are still being investigated.

b. Adenosine triphosphate release: TRPM5-mediated Ca2+ influx opens pannexin hemichannels in the receptor cell membrane. Pannexins are related to the connexins that form gap junctions between cells (see 4·II·F). When pannexins open, they allow ATP to diffuse out of the cell and enter the interstitium. If a receptor potential generated by tastant binding crosses threshold for action potential formation, the cell then generates a train of spikes mediated by voltage-gated Na+ channels. Pannexins are also voltage gated, so spiking potentiates ATP release.

D. Type III cells

Type III cells, which are also known as presynaptic cells, are the only taste receptor cell class to synapse with a sensory nerve. Type III cells sense sour tastes primarily through H+-induced membrane depolarization.

1. Transduction: Sourness is the taste of acid (H+). Common dietary examples include acetate (vinegar), citrate (lemons), and lactate (sour milk). H+ enters cells via ENaC and depolarizes the cell directly, but, once inside the cell, H+ also reduces K+ efflux by inhibiting K+ channels (Figure 10.4). Inhibition further amplifies the depolarization caused by H+ entry.

2. Transmission: If sufficiently large, the H+-induced receptor potential activates voltage-dependent Na+ channels in the cell membrane and triggers a spike. Voltage-dependent Ca2+ channels then open to allow Ca2+ influx and transmitter release (5- hydroxytryptamine [5-HT], also known as serotonin) at a synapse with a sensory afferent neuron.

E. Signal integration

Food contains a mix of different tastants, and, hence, taste bud output usually represents an integrated response to simultaneous stimulation of all three taste cell classes. Type III cells are the only receptors that make synaptic contact with an afferent nerve, but type II cells may also stimulate gustatory nerve activity directly through ATP release (the nerve expresses purinoreceptors), and indirectly by stimulating 5-HT release from type III cells. Type I cells influence the output of the other two receptor cell classes by secreting an ecto-ATPase that terminates signaling.

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Figure 10.4

Type III receptor cell taste transduction. ENaC = epithelial Na+ channel; 5-HT = 5-hydroxytryptamine.

Clinical Application 10.1: Dysgeusia

Taste is a relatively crude sense that serves primarily as a gatekeeper to the gastrointestinal system, causing us to either accept ingested substances as food or reject potentially injurious substances before they are swallowed. Complete loss of taste (ageusia) is uncommon, except in patients with Sjögren syndrome. Sjögren patients suffer from an autoimmune disease that impairs exocrine gland function, including the salivary glands. Saliva is required to carry tastants in dissolved form through the taste bud pore. Metallic dysgeusia (a persistent metallic taste) is a common and troublesome side effect of many antibiotics (e.g., tetracycline and metronidazole) and antifungals.1

F. Taste bud distribution

Taste buds are distributed throughout the oral cavity, although the highest concentrations are located on the dorsal surface of the tongue. Lingual taste buds reside on surface projections called papillae. Three types of papillae can be distinguished based on shape and taste bud density: fungiformfoliate, and circumvallate (Figure 10.5).

1. Fungiform papillae: The anterior portions of the tongue bear fungiform papillae. Each thumblike projection carries a few taste buds at its tip.

2. Foliate papillae: The posterior lateral edge of the tongue bears ridges called foliate papillae. The sides of the papillae are studded with hundreds of taste buds.

3. Circumvallate papillae: The largest concentration of taste buds is found on buttonlike circumvallate papillae. They are located in a line across the back of the tongue.

G. Neural pathways

Taste buds are innervated by three different cranial nerves (CNs). The tongue's anterior portions and the palate are innervated by the facial nerve (CN VII). Taste buds on the posterior tongue signal via the glossopharyngeal nerve (CN IX), whereas the vagus (CN X) innervates the pharynx and larynx. All three nerves relay information via the tractus solitarius to a gustatory area within the solitary nucleus (brainstem). Secondary fibers carry gustatory information to the thalamus and primary gustatory cortex.

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Figure 10.5

Taste bud distribution on the tongue surface.

image 1More information on these drugs can be found in LIR Pharmacology, 5e, p. 442.

III. SMELL

The human sense of smell is not as well developed as that in many animals, but, even so, the human olfactory system is capable of distinguishing hundreds of thousands of different odors. Olfactory sensitivity relies on several hundred unique receptors, each encoded by a different gene.

A. Receptors

Odorants are airborne chemicals that are inhaled and carried through the nasal passages during normal breathing or by intentional sniffing. Odors are detected and transduced by chemoreceptors that belong to the GPCR superfamily. The human genome contains ~900 different olfactory receptor genes, of which ~390 are functionally expressed.

B. Receptor cells

Odorant receptors are expressed on cilia that project from sensory neurons contained within a specialized olfactory epithelium that lines the roof of the nasal cavity (Figure 10.6). The sensory neurons are bipolar. The apical portion of the cell body gives rise to a single dendrite that extends toward the epithelial surface and then terminates in a swelling (olfactory knob). Each knob supports 10–30 long, nonmotile, sensory cilia which project into a thin layer of watery mucus. The mucus traps passing odorant molecules and allows them to be detected by odorant receptors.

C. Transduction

Odorant binding to its receptor activates an olfactory-specific G protein (Golf) and initiates an adenylyl cyclase–mediated rise in intracellular cAMP concentration (Figure 10.7). A cAMP-gated ion channel opens as a result, allowing Na+ and Ca2+ influx. The Ca2+ flux, in turn, opens a Ca2+-dependent Cl channel, and the combined depolarizing effect of cation influx and anion efflux on membrane potential may be sufficient to trigger a spike in the olfactory neuron.

D. Olfactory epithelium

Olfactory receptor neurons have an average lifespan of ~48 days and then are replaced. Receptor neurons are formed from olfactory epithelial basal cells, which are neuroblast stem cells. The epithelium also contains supporting cells, which have a glia-like function. The mucus that flows over the epithelium is secreted by Bowman glands. Olfactory mucus contains odorant-binding proteins that help ferry hydrophobic odorants to the olfactory receptors. Mucus also contains lactoferrin, lysozyme, and various immunoglobulins that help ensure that pathogens do not gain access to the central nervous system (CNS) via olfactory nerves. The olfactory epithelium is one of the few regions of the body where CNS nerves directly interface with the external environment.

Clinical Application 10.2: Anosmia

Although an inability to detect odors caused by food spoilage can increase the likelihood of food poisoning, loss of the sense of smell (anosmia) is not life threatening. Anosmia does significantly impact the quality of life, however. Anosmia markedly impairs food enjoyment and often causes appetite and weight loss, depression, and withdrawal from social events that involve food. Hyposmia commonly occurs during aging and as a result of upper respiratory tract infections. Neurodegenerative diseases (Parkinson and Alzheimer disease) can also impair sense of smell. Anosmia may often follow head trauma as a result of damage to the olfactory cortex or shearing of the olfactory nerves as they pass through the cribriform plate.

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Figure 10.6

Olfactory epithelium.

E. Neural pathways

Olfactory receptor cells are primary sensory neurons that project directly to the olfactory bulb, which is an extension of the forebrain. Axons from the sensory neurons form bundles and then pass through foramina in the cribriform plate of the ethmoid bone. Axons travel in the olfactory nerve (CN I) to the glomerulus of the olfactory bulb, where they synapse. Neurons originating in the olfactory bulb project to several brain regions, including the olfactory cortex, the thalamus, and the hypothalamus. Individual olfactory neurons express a single receptor gene. Because the number of odorants that a person can distinguish exceeds receptor gene number by several orders of magnitude, the receptors must recognize specific chemical groups of multiple odorant molecules rather than responding to just one odorant. The brain then extrapolates a unique odor signature based on relative output intensity from each of the different receptor types within the olfactory receptor array.

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Figure 10.7

Olfactory transduction. cAMP = cyclic adenosine monophosphate; Golf = olfactory-specific G protein.

Chapter Summary

• Gustation and olfaction (taste and smell) allow us to detect chemicals in food and in inhaled air. Taste is used largely to decide whether or not to swallow ingested food. Olfaction allows for an appreciation of food as well as detection of pheromones.

• There are five basic tastes: saltysweetumami (savory), bitter, and sour.

• Taste receptor cells reside in taste buds found throughout the oral cavity. Type I receptors are glia-like cells that transduce salty taste (Na+). Na+ excites type I cells by permeating an epithelial Na+ channel. Type I cells also help terminate gustatory signaling.

• Type II cells express tastant-specific G protein–coupled receptors (GPCRs) that detect sweet, umami, and bitter tastes. The GPCRs act through gustducin, a taste cell–specific G protein. The activated Gβγsubunit elicits intracellular Ca2+ release and depolarization. Pannexin hemichannels in the surface membrane then open and allow adenosine triphosphate (ATP) to diffuse out of the cell. ATP stimulates sensory afferent neurons both directly and indirectly by modulating type III cell output.

• Type III cells transduce the sour taste of acid. H+ permeates an epithelial Na+ channel and causes receptor depolarization. Type III cells are innervated by gustatory nerves and signal excitation to the afferents via 5-hydroxytryptamine (serotonin) release.

• Odors are detected by an olfactory epithelium located in the roof of the nasal cavity. Olfactory receptors are G protein–coupled receptors expressed on the surface of cilia that project into a mucus layer lining the olfactory epithelium.

• Olfactory receptor cells are bipolar central neurons that relay information to the olfactory bulb. Olfactory receptor binding triggers a cyclic adenosine monophosphate (cAMP)-mediated signaling cascade that leads to cAMP-dependent Ca2+ influx and Ca2+-dependent Cl efflux and causes nerve excitation.



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