After studying this chapter, you should be able to:
Describe the basic features of the neural elements in the olfactory epithelium and olfactory bulb.
Describe signal transduction in odorant receptors.
Outline the pathway by which impulses generated in the olfactory epithelium reach the olfactory cortex.
Describe the location and cellular composition of taste buds.
Name the five major taste receptors and signal transduction mechanisms in these receptors.
Outline the pathways by which impulses generated in taste receptors reach the insular cortex.
Smell (olfaction) and taste (gustation) are generally classified as visceral senses because of their close association with gastrointestinal function. Physiologically, they are related to each other. The flavors of various foods are in large part a combination of their taste and smell. Consequently, food may taste “different” if one has a cold that depresses the sense of smell. Both smell and taste receptors are chemoreceptors that are stimulated by molecules in solution in mucus in the nose and saliva in the mouth. Because stimuli arrive from an external source, they are also classified as exteroceptors. The sensations of smell and taste allow individuals to distinguish between estimates of up to 30 million compounds that are present in food, predators, and mates and to convert the information received into appropriate behaviors.
OLFACTORY EPITHELIUM AND OLFACTORY BULBS
Olfactory sensory neurons are located in a specialized portion of the nasal mucosa, the yellowish pigmented olfactory epithelium. In dogs and other animals in which the sense of smell is highly developed (macrosmatic animals), the area covered by this membrane is large; in microsmatic animals, such as humans, it is small. In humans, it covers an area of 10 cm2 in the roof of the nasal cavity near the septum (Figure 11–1). The olfactory epithelium is said to be the place in the body where the nervous system is closest to the external world.
FIGURE 11–1 Structure of the olfactory epithelium. There are three cell types: olfactory sensory neurons, supporting (sustentacular) cells, and basal stem cells at the base of the epithelium. Each olfactory sensory neuron has a dendrite that projects to the epithelial surface. Numerous cilia protrude into the mucus layer lining the nasal lumen. Odorants bind to specific odorant receptors on the cilia and initiate a cascade of events leading to generation of action potentials in the sensory axon. Each olfactory sensory neuron has a single axon that projects to the olfactory bulb, a small ovoid structure that rests on the cribriform plate of the ethmoid bone. (From Kandel ER, Schwartz JH, Jessell TM [editors]: Principles of Neural Science, 4th ed. McGraw-Hill, 2000.)
The human olfactory epithelium contains about 50 million bipolar olfactory sensory neurons interspersed with glia-like supporting (sustentacular) cells and basal stem cells. New olfactory sensory neurons are generated by basal stem cells as needed to replace those damaged by exposure to the environment. The olfactory epithelium is covered by a thin layer of mucus secreted by the supporting cells and Bowman glands, which lie beneath the epithelium.
Each olfactory sensory neuron has a short, thick dendrite that projects into the nasal cavity where it terminates in a knob containing 6–12 cilia (Figure 11–1). In humans, the cilia are unmyelinated processes, about 5–10 μm long and 0.1–2 μm in diameter that protrude into the mucus overlying the epithelium. Odorant molecules (chemicals) dissolve in the mucus and bind to odorant receptors on the cilia of olfactory sensory neurons. The mucus provides the appropriate molecular and ionic environment for odor detection.
The axons of the olfactory sensory neurons (first cranial nerve) pass through the cribriform plate of the ethmoid bone and enter the olfactory bulbs (Figure 11–1). In the olfactory bulbs, the axons of the olfactory sensory neurons contact the primary dendrites of the mitral cells and tufted cells (Figure 11–2) to form anatomically discrete synaptic units called olfactory glomeruli. The olfactory bulbs also contain periglomerular cells, which are inhibitory neurons connecting one glomerulus to another, and granule cells, which have no axons and make reciprocal synapses with the lateral dendrites of the mitral and tufted cells (Figure 11–2). At these synapses, the mitral or tufted cells excite the granule cell by releasing glutamate, and the granule cells in turn inhibit the mitral or tufted cell by releasing GABA.
FIGURE 11–2 Basic neural circuits in the olfactory bulb. Note that olfactory receptor cells with one type of odorant receptor project to one olfactory glomerulus (OG) and olfactory receptor cells with another type of receptor project to a different olfactory glomerulus. Solid black arrows signify inhibition via GABA release, and white arrows signify excitatory connections via glutamate release. CP, cribriform plate; Gr, granule cell; M, mitral cell; PG, periglomerular cell; T, tufted cell. Gr, granule cell. (Adapted with permission from Mori K, et al: The olfactory bulb: coding and processing of odor molecular information. Science 1999;286(5440):711–715.)
Free endings of many trigeminal pain fibers are found in the olfactory epithelium. They are stimulated by irritating substances, which leads to the characteristic “odor” of such substances as peppermint, menthol, and chlorine. Activation of these endings by nasal irritants also initiates sneezing, lacrimation, respiratory inhibition, and other reflexes.
The tufted cells are smaller than the mitral cells and they have thinner axons, but they are similar from a functional point of view. The axons of the mitral and tufted cells pass posteriorly through the lateral olfactory stria to terminate on apical dendrites of pyramidal cells in five regions of the olfactory cortex: anterior olfactory nucleus, olfactory tubercle, piriform cortex, amygdala, and entorhinal cortex (Figure 11–3). From these regions, information travels directly to the frontal cortex or via the thalamus to the orbitofrontal cortex. Conscious discrimination of odors is dependent on the pathway to the orbitofrontal cortex. The orbitofrontal activation is generally greater on the right side than the left; thus, cortical representation of olfaction is asymmetric. The pathway to the amygdala is probably involved with the emotional responses to olfactory stimuli, and the pathway to the entorhinal cortex is concerned with olfactory memories.
FIGURE 11–3 Diagram of the olfactory pathway. Information is transmitted from the olfactory bulb by axons of mitral and tufted relay neurons in the lateral olfactory tract. Mitral cells project to five regions of the olfactory cortex: anterior olfactory nucleus, olfactory tubercle, piriform cortex, and parts of the amygdala and entorhinal cortex. Tufted cells project to anterior olfactory nucleus and olfactory tubercle; mitral cells in the accessory olfactory bulb project only to the amygdala. Conscious discrimination of odor depends on the neocortex (orbitofrontal and frontal cortices). Emotive aspects of olfaction derive from limbic projections (amygdala and hypothalamus). (From Kandel ER, Schwartz JH, Jessell TM [editors]: Principles of Neural Science, 4th ed. McGraw-Hill, 2000.)
In rodents and various other mammals, the nasal cavity contains another patch of olfactory epithelium located along the nasal septum in a well-developed vomeronasal organ. This structure is concerned with the perception of odors that act as pheromones. Vomeronasal sensory neurons project to the accessory olfactory bulb (Figure 11–3) and from there to the amygdala and hypothalamus that are concerned with reproduction and ingestive behavior. Vomeronasal input has major effects on these functions. An example is pregnancy block in mice; the pheromones of a male from a different strain prevent pregnancy as a result of mating with that male, but mating with a mouse of the same strain does not produce blockade. The vomeronasal organ has about 100 G protein-coupled odorant receptors that differ in structure from those in the rest of the olfactory epithelium.
The organ is not well developed in humans, but an anatomically separate and biochemically unique area of olfactory epithelium occurs in a pit in the anterior third of the nasal septum, which appears to be a homologous structure. There is evidence for the existence of pheromones in humans, and there is a close relationship between smell and sexual function. Perfume advertisements bear witness to this. The sense of smell is said to be more acute in women than in men, and in women it is most acute at the time of ovulation. Smell, and to a lesser extent, taste, have a unique ability to trigger long-term memories, a fact noted by novelists and documented by experimental psychologists.
ODORANT RECEPTORS AND SIGNAL TRANSDUCTION
The olfactory system has received considerable attention in recent years because of the intriguing biologic question of how a simple sense organ such as the olfactory epithelium and its brain representation, which apparently lacks a high degree of complexity, can mediate discrimination of more than 10,000 different odors. One part of the answer to this question is that there are many different odorant receptors.
There are approximately 500 functional olfactory genes in humans, accounting for about 2% of the human genome. The amino acid sequences of odorant receptors are very diverse, but all the odorant receptors are G protein coupled receptors (GPCR). When an odorant molecule binds to its receptor, the G protein subunits (α, β, γ) dissociate (Figure 11–4). The α-subunit activates adenylate cyclase to catalyze the production of cAMP, which acts as a second messenger to open cation channels, increasing the permeability to Na+, K-, and Ca2+. The net effect is an inward-directed Ca2+ current which produces the graded receptor potential. This then opens Ca2+-activated Cl-channels, further depolarizing the cell due to the high intracellular Cl- levels in olfactory sensory neurons. If the stimulus is sufficient for the receptor potential to exceed its threshold, an action potential in the olfactory nerve (first cranial nerve) is triggered.
FIGURE 11–4 Signal transduction in an odorant receptor. A) Olfactory receptors are examples of G protein-coupled receptors; ie, they are associated with three G protein subunits (α, β, γ).
B) When an odorant binds to the receptors, the subunits dissociate.
A second part of the answer to the question of how 10,000 different odors can be detected lies in the neural organization of the olfactory pathway. Although there are millions of olfactory sensory neurons, each expresses only one of the 500 olfactory genes. Each neuron projects to one or two glomeruli (Figure 11–2). This provides a distinct two-dimensional map in the olfactory bulb that is unique to the odorant. The mitral cells with their glomeruli project to different parts of the olfactory cortex.
The olfactory glomeruli demonstrate lateral inhibition mediated by periglomerular cells and granule cells. This sharpens and focuses olfactory signals. In addition, the extracellular field potential in each glomerulus oscillates, and the granule cells appear to regulate the frequency of the oscillation. The exact function of the oscillation is unknown, but it probably also helps to focus the olfactory signals reaching the cortex.
ODOR DETECTION THRESHOLD
Odor-producing molecules (odorants) are generally small, containing from 3 to 20 carbon atoms; and molecules with the same number of carbon atoms but different structural configurations have different odors. Relatively high water and lipid solubility are characteristic of substances with strong odors. Some common abnormalities in odor detection are described in Clinical Box 11–1.
CLINICAL BOX 11–1
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, 1–2% 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 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.
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.
The odor detection thresholds are the lowest concentration of a chemical that can be detected. The wide range of thresholds illustrates the remarkable sensitivity of the odorant receptors. Some examples of substances detected at very low concentrations include hydrogen sulfide (0.0005 parts per million, ppm), acetic acid (0.016 ppm), kerosene (0.1 ppm), and gasoline (0.3 ppm). On the other end of the spectrum, some toxic substances are essentially odorless; they have odor detection thresholds higher than lethal concentrations. An example is carbon dioxide, which is detected at 74,000 ppm but is lethal at 50,000 ppm. Not all individuals have the same odor detection threshold for a given odorant. While one person may detect and recognize an odorant at a particular concentration, another person may barely notice it.
Olfactory discrimination is remarkable. On the other hand, determination of differences in the intensity of any given odor is poor. The concentration of an odor-producing substance must be changed by about 30% before a difference can be detected. The comparable visual discrimination threshold is a 1% change in light intensity. The direction from which a smell comes may be indicated by the slight difference in the time of arrival of odorant molecules in the two nostrils.
The olfactory epithelium contains one or more odorant-binding proteins (OBP) that are produced by support cells and released onto the extracellular space. An 18-kDa OBP that is unique to the nasal cavity has been isolated, and other related proteins probably exist. The protein has considerable homology to other proteins in the body that are known to be carriers for small lipophilic molecules. A similar binding protein appears to be associated with taste. These OBP may function in several ways. One, they may concentrate the odorants and transfer them to the receptors. Two, they may partition hydrophobic ligands from the air to an aqueous phase. Three, they may sequester odorants away from the site of odor recognition to allow for odor clearance.
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/calmodulin-dependent protein kinase II acting on adenylyl cyclase. The next step is called long-term adaptation, which includes activation of guanylate cyclase and cGMP production. A Na+/Ca2+ exchanger to restore ion balance also contributes to long-term adaptation.
The specialized sense organ for taste (gustation) consists of approximately 10,000 taste buds, which are ovoid bodies measuring 50–70 μm. There are four morphologically distinct types of cells within each taste bud: basal cells, dark cells, light cells, and intermediate cells (Figure 11–5). 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.
FIGURE 11–5 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 from Kandel ER, Schwartz JH, Jessell TM [editors]: Principles of Neural Science, 4th ed. McGraw-Hill, 2000.)
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 11–5). 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’s glands (also called gustatory glands or serous glands) secrete saliva 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’s glands form a functional complex that is important in actual taste detection because of the enzymes secreted by the gland.
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 brain stem via the glossopharyngeal nerve (Figure 11–6). 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 11–6). 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.
FIGURE 11–6 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 from Kandel ER, Schwartz JH, Jessell TM [editors]: Principles of Neural Science, 4th ed. McGraw-Hill, 2000.)
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 11–7. They include the two major types of receptors: ligand-gated channels (ionotropic receptors) and GPCR (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 GPCR in the human genome are taste receptors (T1R and T2R families). In some cases, these receptors couple to the heterotrimeric G protein, gustducin. Gustducin lowers cAMP and increases the formation of inositol phosphates (IP3), which can lead to depolarization.
FIGURE 11–7 Signal transduction in taste receptors. Salt-sensitive taste is mediated by a Na+-selective channel (ENaC); sour taste is mediated by H+ ions permeable via ENaCs; sweet taste may be dependent on the T1R3 family of G protein-coupled receptors which couple to the G protein gustducin; bitter taste is mediated by the T2R family of G protein-coupled receptors; umami taste is mediated by glutamate acting on a metabotropic receptor, mGluR4. (Adapted with permission from Lindemann B: Receptors and transduction in taste. Nature 2001:413(6852):219–225.)
The salty taste is triggered by NaCl. Salt-sensitive taste is mediated by a Na+-selective channel known as ENaC, the amiloride-sensitive epithelial sodium channel. The entry of Na+ into the salt receptors depolarizes the membrane, generating the receptor potential. In humans, the amiloride sensitivity of salt taste is less pronounced than in some species, suggesting that there are additional mechanisms to activate salt-sensitive receptors.
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, HCN, a hyperpolarization-activated cyclic nucleotide-gated cation channel, and other mechanisms may contribute to sour transduction.
Substances that taste sweet act via the G protein gustducin. The T1R3 family of GPCR is expressed by about 20% of taste cells, some of which also express gustducin. 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. Sweet-responsive 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 GPCR (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.
TASTE THRESHOLDS & INTENSITY DISCRIMINATION
The ability of humans to discriminate differences in the intensity of tastes, like 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 11–1). 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.
TABLE 11–1. Some taste thresholds.
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 11–5) 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 11–2.
CLINICAL BOX 11–2
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 amoeboid 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 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 a 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.
Improved oral hygiene and adding zinc supplements to one’s diet can correct the inability to taste in some individuals.
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.
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 comprised of basal stem cells and three types of taste cells (dark, light, and intermediate cells). 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 GPCR 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 nucleus of the tractus solitarius. From there, axons ascend via the ipsilateral medial lemniscus to the ventral posteromedial nucleus of the thalamus, and on to the anterior insula and frontal operculum in the ipsilateral cerebral cortex.
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.
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 β-arrestin content in olfactory neurons.
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
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 GPCR : 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 physician, 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.
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 brain stem 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
Adler E, Melichar JK, Nutt DJ, et al: A novel family of mammalian taste receptors. Cell 2000;100:693.
Anholt RRH: Odor recognition and olfactory transduction: The new frontier. Chem Senses 1991;16:421.
Bachmanov AA, Beauchamp GK: Taste receptor genes. Annu Rev Nutrition 2007;27:389.
Gilbertson TA, Damak S, Margolskee RF: The molecular physiology of taste transduction. Curr Opin Neurobiol 2000;10:519.
Gold GH: Controversial issues in vertebrate olfactory transduction. Annu Rev Physiol 1999;61:857.
Heath TP, Melichar JK, Nutt DJ, Donaldson LF. Human taste thresholds are modulated by serotonin and noradrenaline. J Neurosci 2006;26:12664.
Herness HM, Gilbertson TA: Cellular mechanisms of taste transduction. Annu Rev Physiol 1999;61:873.
Kato A, Touhara K. Mammalian olfactory receptors: pharmacology, G protein coupling and desensitization. Cell Mol Life Sci 2009;66:3743.
Lindemann B: Receptors and transduction in taste. Nature 2001;413:219.
Mombaerts P: Genes and ligands for odorant, vomeronasal and taste receptors. Nature Rev Neurosci 2004;5:263.
Reisert J, Restrepo D: Molecular tuning of odorant receptors and its implication for odor signal processing. Chem Senses 2009;34:535.
Ronnett GV, Moon C: G proteins and olfactory signal transduction. Annu Rev Physiol 2002;64:189.
Shepherd GM, Singer MS, Greer CA: Olfactory receptors: A large gene family with broad affinities and multiple functions (Review). Neuroscientist 1996;2:262.
Stern P, Marks J (editors): Making sense of scents. Science 1999;286:703.