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Learning Objectives
After completing this chapter, you should be able to:
• Name the somatosensory receptors located in the skin, muscles, joints, and tendons and explain the function of each type of receptor.
• Differentiate among the somatosensations of kinesthesia, proprioception, and interoception. • List the differences between the lemniscal and extralemniscal somatosensory systems. • Describe the somatosensory disorders associated with damage to the “What” and “Where” streams in the
secondary somatosensory cortex. • Explain the Gate-Control Theory of Pain. • Give the rationale for various treatments for pain, including drugs, counterirritation, acupuncture, trans-
cutaneous electrical nerve stimulation, and hypnosis. • Draw an illustration of the location of primary and accessory olfactory receptors in the nasal cavity and trace
their pathways to the brain. • List the possible causes of olfactory disorders. • Explain the physical bases for the five primary tastes: sweet, sour, salty, bitter, and umami. • Trace the pathway of taste information from taste receptors to the cerebrum. • Differentiate between ageusia and dysgeusia. • Compare the function of the hair cells in the utricles, saccules, and semicircular canals. • Enumerate the different pathways that carry information from the hair cells in the vestibular system to
various structures in the central nervous system. • Identify the disorders associated with the vestibular system.
7
Taste, Smell, and the Body Senses
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CHAPTER 7Section 7.1 The Somatosensory System
Max is a 4-year-old boy who is autistic. Like many children with autism, Max tends to ignore oth- ers in his family, even when they call his name, and avoids looking at their faces. His language is delayed, and he shows little interest in pretend play or toys. Also, Max is afraid of toys that produce even the slightest vibrations. If a vibrating object is placed against his skin, he will overreact by yell- ing, crying, hitting, and running away to escape from the vibrating object.
In fact, most light touch causes Max to have a meltdown. He puts up a fight when his mother tries to dress him because he doesn’t like the feel of clothing on his skin. The seams of his shirts, the elastic in his underwear and socks, and tags on his clothing send him into a howling rage. Even the wind on his face is aversive to him.
On the other hand, Max doesn’t mind deep pressure on his skin. His behavior therapist has taught Max’s parents to use a firm grip on his arm or leg to calm him down. Max bangs his forehead on the floor or on the headboard of his bed when he is bored. This pounding doesn’t appear to bother him at all.
Not all autistic children react to light stimulation of the skin like Max does. Some enjoy the sensation of light touch and vibrations, and they can become quite fixated on objects that stroke the skin or produce vibrations. Some react violently to deep pressure on the skin, a sensation that Max appears to like. Other children with autism react normally to light and deep pressure on the skin.
The sense of touch is designed to provide information about the outside world and, thus, plays a protective role. However, Max’s brain developed abnormally, producing his autistic symptoms such as his oversensitivity to light touch. Max has a sensory disorder in which the brain may incor- rectly process the sensation of touch as a dangerous signal, resulting in Max’s defensive reaction when his skin is touched lightly. In Chapter 13 we will discuss normal and abnormal brain devel- opment. In this chapter we will explore the role of touch and other senses in informing us about what is going on inside and outside of our bodies. Let’s begin by examining the sense of touch, which is one of several senses that are classified as body senses or somatosensations.
7.1 The Somatosensory System
The root of the word somatosensory is soma, which means “body” in Greek. Thus, the somato-sensory system relays information about the body to the brain. Somatosensory receptors include receptors in the skin as well as receptors in muscles, joints, and tendons. Therefore, the somatosensory system comprises skin senses and the senses of kinesthesia, proprioception, and interoception. The word kine means “to move” in Greek. Hence, kinesthesia refers to the ability to sense movement. Proprioception is the ability to know where a body part is in space. Recall from Chapter 2 that many body organs are lined with smooth muscles, which contain somato- sensory receptors that inform the brain when stretching takes place in the muscle. Thanks to our somatosensory system, we can tell when our stomachs are full and when our bladders are in need of emptying. This sensation from internal organs is called interoception.
The Nature of Somatosensory Stimuli
Most somatosensory receptors are mechanoreceptors, which means that they respond to physi- cal forces like pulling or stretching. Stretching of a muscle excites the stretch receptors in that muscle. On the other hand, stretching of the tendon stimulates stretch receptors in tendons.
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CHAPTER 7Section 7.1 The Somatosensory System
Recall that Helen Keller could sense vibrations through her skin. The receptors in the skin pro- vide information about pressure, temperature, and pain. Vibration is nothing more than a rapidly repeating pattern of momentary pressure on the skin. Pressure and vibration directly stimulate mechanoreceptors. Temperature can also stimulate mechanoreceptors because cold causes shrinkage of tissue, and warmth produces expansion. However, temperature changes can also affect chemoreceptors because some chemicals such as enzymes are active at certain tempera- tures but not at others.
Pain, too, can be relayed to the brain by way of chemoreceptors and mechanoreceptors. Cer- tainly, too much pressure on the skin, as when the skin is pinched, can produce pain. But certain stimuli, such as a bee sting, produce pain indirectly through chemoreceptors. A bee sting causes the release of chemicals that stimulate chemoreceptors, which send pain signals to the brain.
Anatomy and Function of the Somatosensory System
Numerous receptors are found in the skin. Figure 7.1 illustrates the many varieties of receptors located in the skin. Pacinian corpuscles are skin receptors that consist of a central sensory fiber surrounded by concentric layers of tissue. These receptors appear to respond to pressure. Other receptors include Ruffini’s endings, Krause’s end-bulbs, Meissner’s corpuscles, Merkel’s disks, bas- ket cells, and free nerve endings.
Figure 7.1: Anatomy of the sensory receptors in the skin
This diagram shows the different components that are parts of the system of sensory receptors in the skin. Each part performs a specific job so that the skin functions properly and provides a rich complex of sensations.
Epidermis
Dermis
Duct of sweat gland
Free nerve endings
Merkel’s disks (touch)
Meissner’s corpuscle (touch)
Ruffini’s ending
Pacinian corpuscle
Free nerve ending Fat globules
Krause’s end-bulbs
Muscle
Sebaceous gland
Hair
Nerve ending around hair
(basket ending)
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CHAPTER 7Section 7.2 Somatosensory Processing
The functions of many of these are not clear. There is evidence that free nerve endings respond to painful stimuli, although any receptor can produce the sensation of pain if it is overstimulated. In addition, Ruffini’s endings appear to respond to warm stimuli, and Krause’s end-bulbs are excited by cold stimuli. However, many areas on the body lack Ruffini’s or Krause’s receptors, yet these areas still respond to warm or cold stimuli. Thus, Ruffini’s endings and Krause’s end-bulbs may transmit information about temperature to the brain, but they are not necessary for the sensation of temperature. Sound confusing? I assure you that it is confusing, even for experts in the area of somatosensation.
The stretch receptors located in muscles, tendons, and joints send information to the brain about stretching. That is, when a muscle or tendon or joint is stretched, action potentials are transmitted to the brain. The brain, in turn, uses this information to create a body image of which muscles are contracted, which muscles are relaxed, and which limbs are bent or straight. You can tell where your limbs are in space, even when your eyes are closed. This is the essence of body image: know- ing the position of all of your body parts without visually checking. Kinesthesia and proprioception work together to produce one’s body image.
Two separate pathways, the lemniscal pathway and the extralemniscal pathway, carry information about somatosensation to the brain. The lemniscal pathway relays information about pressure and stretching to the brain by way of A-fibers, which are myelinated axons that have a large diam- eter. In contrast, the extralemniscal pathway relays information about pain and temperature by way of thin, unmyelinated axons called C-fibers. Recall from Chapter 2 that action potentials travel very rapidly down thick, myelinated axons, and they move most slowly down thin, unmyelinated axons. Therefore, information about pressure and stretch travels quickly to the brain, and informa- tion about pain and temperature is relayed more slowly.
Have you ever stepped into a bathtub filled with hot water? At first you are not aware of the water’s temperature. But after a second or two, the sensation of warmth builds in your foot and eventually feels so hot that you withdraw your foot from the water. Sensations of pain and tem- perature are quite primitive and developed before touch sensations. Thus, they travel to the brain by way of evolutionarily older pathways, those without myelin.
7.2 Somatosensory Processing
Imagine that a fly lands on your left arm while you are reading. You don’t see it or hear it, but you know the fly is there because you can feel it on your skin. Without looking at it, you can tell that it is very light, almost weightless. You can also feel its movement up your arm, from your wrist to just below your elbow. Immediately, you perceive that there is an insect on your arm (“What”), and you swat at it with your right hand (“Where”).
The sensations that arise from the body are transmitted to the brain by way of the somatosensory system. This information, especially from the skin and muscles, is important because it tells us about the location of our limbs in space and about objects in the environment that are touching us. Recall that somatosensory information travels to the brain by way of two pathways: the lem- niscal pathway and the extralemniscal pathway. This information, after passing through several synapses in the midbrain and thalamus, is projected to the primary somatosensory cortex in the parietal lobe (Figure 7.2).
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CHAPTER 7Section 7.2 Somatosensory Processing
Figure 7.2: Primary and secondary somatosensory areas
The primary and secondary somatosensory areas are located in the parietal lobe. Like the motor cortex, the primary somatosensory cortex is topographically organized.
You were introduced to the primary somatosensory cortex in Chapter 1. Recall that it is topo- graphically organized, with each neuron in the primary somatosensory cortex receiving informa- tion from a specific area of the body. For example, information from the big toe on my right foot goes to neurons in the upper aspect of my left postcentral gyrus, and information from the left side of my face goes to neurons in the lower aspect of my right postcentral gyrus (Figure 7.2). Studies of brain-injured individuals and single-cell recordings in the brains of macaque monkeys have revealed that somatosensory information is processed along “What” and “Where” streams, much like the visual and auditory systems (Reed, Caselli, & Farah, 1996). Information received by the primary somatosensory cortex is sent on to other cortical regions, collectively known as the secondary somatosensory cortex, for “What” and “Where” processing.
Damage to the inferior parietal cortex produces a disorder called tactile agnosia, in which the affected individuals cannot recognize objects through touch (Caselli, 1991; Reed & Caselli, 1994; Valenza et al., 2001). Agnosia means without knowledge (gnos means “knowledge” in Greek). The affected individuals perform well on tests of spatial ability and can recognize the objects visually. In addition, there is no impairment of their ability to detect tactile stimuli. However, when asked to identify an object through the sense of touch, people with damage to the inferior parietal cor- tex can accurately judge the length and size of the object, but they cannot recognize it. Therefore, the “What” system appears to be associated with the inferior parietal cortex. The word inferior means “below” or “bottom.” Thus, the inferior parietal cortex is located at the bottom or lowest region of the parietal lobe (Figure 7.2).
The posterior parietal cortex processes “Where” information from the somatosensory system. Recall that this area of the cortex also receives “Where” information from the visual system (Duhamel, Colby, & Goldberg, 1998; Graziano, Cooke, & Taylor, 2000). This area processes visual and somatosensory input simultaneously to produce a sense of “body image” that guides
Occipital lobe
Parietal lobe
Somatosensory cortex (primary)
Motor cortex
Prefrontal area
A. Cerebrum (top view)
Genitals
Foot
Leg
Hip
Trunk Neck Head Shoulder Arm
Hand Fingers Thumb
Eye Nose Face
Lips
Teeth Tongue Pharynx Abdomen
B. Primary somatosensory cortex
Somatosensory cortex
(secondary)
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CHAPTER 7Section 7.2 Somatosensory Processing
movement and body postures, like sitting or standing. Movement of tactile stimuli across the skin, as well as the location of the stimuli and their spatial relationship to other tactile stimuli, is pro- cessed in the posterior parietal lobe.
Plasticity of the Somatosensory Cortex
A number of investigators have demonstrated that the topographical map of the primary somato- sensory cortex is quite plastic and can be reorganized. For example, specific tactile experiences can change the organization of the somatosensory cortex. Recordings of brain activity of blind individuals revealed that the fingertip used for reading Braille sends input to a larger area of the somatosensory cortex than do the fingers not used for reading (Pascual-Leone & Torres, 1993). In addition, the fingers on the left hands of violinists activate larger areas on the primary somatosen- sory cortex than do the fingers of nonmusicians, as brain activity recordings have shown (Elbert, Pantev, Weinbruch, Rockstroh, & Taub, 1995).
The topographical organization of the primary somatosensory cortex is also altered following amputation of a limb (Florence, Taub, & Kaas, 1998; Merzenich, 1998; Ramachandran & Blakeslee, 1998; Ramachandran & Hirstein, 1998; Ramachandran & Rogers-Ramachandran, 2000; Ramach- andran, Brang, & McGeoch, 2010). That is, the neurons in the postcentral gyrus that formerly received input from the missing limb come to respond to receptors located in the trunk and face, as well as the stump of the amputated limb (Figure 7.3). The end result is that a touch on the face of an individual with an amputated limb will induce a sensation that feels as if it is coming from the missing limb (Ramachandran, Rogers-Ranachandran, & Stewart, 1992). This large-scale reorgani- zation of the primary somatosensory cortex is not well understood (Paullus & Hickmott, 2011).
Figure 7.3: Reorganization of the primary somatosensory cortex following amputation of an arm
Following amputation of an arm, areas of the primary somatosensory cortex that formerly responded to sensations in the arm will come to respond to sensations in the leg, trunk, and face.
Reprinted with permission from Merzenich, M. (1998). Reorganization of the primary somatosensory cortex following amputation of an arm. Science, 282, 1063. Illus. K. Sutliff. Copyright . 1998 American Association for the Advancement of Science.
Proximal arm/trunk/leg
Face
Distal arm/hand
Normal Amputee
Body sensation
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CHAPTER 7Section 7.2 Somatosensory Processing
However, the ability of the primary somatosensory cortex to reorganize may contribute to the experience of chronic pain, especially a type of chronic pain known as phantom limb pain, in which an individual who has had a limb amputated continues to feel pain in the missing limb long after it has been amputated. Phantom limb pain is seen in many individuals who have suffered amputation of a limb. Flor and his colleagues (1998) discovered that the severity of phantom limb pain experienced is directly related to the extent of the reorganization of the somatosensory cor- tex, with more pain being associated with greater reorganization within the cortex. To understand this finding, let’s examine the cortical processes responsible for the perception of pain.
Perception of Pain
Have you ever noticed that an ache or pain hurts worse when you are hungry or tired? The sensa- tion of pain results from a complex interplay of signals from pain receptors and inhibitory mes- sages that descend from the brain. That is, the experience of pain is influenced by many factors, including a person’s level of motivation, attitude toward and expectations about pain, and atten- tion paid to the painful stimulus. The amount of tissue damage, by itself, does not predict the amount of pain felt. The intensity of pain perceived depends on the pattern of action potentials generated by pain receptors and the amount of inhibition that is generated by specific areas of the brain stem and cerebral cortex.
Melzack and Wall (1965) were the first investigators to explain the curious observation that people respond in different ways to identically painful stimuli. Their explanation is called the Gate-Control Theory of Pain (Figure 7.4). According to this theory, C-fibers carry information about pain to neurons in the substantia gelatinosa, which is located in the spinal cord and extends into the medulla. From the substantia gelatinosa, information about pain is relayed to the brain stem and on to the cerebral cortex, where pain is consciously experienced. However, pain messages can be prevented from reaching the cortex by “closing the gate,” a metaphor that Melzack and Wall used to describe the influence of certain brain structures and A-fibers to block pain messages flowing to the brain (Melzack & Wall, 1965). Areas of the brain stem send axons down to the substantia gelatinosa, which release endorphins that inhibit transmission of pain information to the brain. A-fibers that carry tactile information can also “close the gate” to stop pain information from reaching the brain.
Neurochemical Explanation of the Gate-Control Theory Pain receptors use a neurotransmitter known as substance P to signal the presence of tissue dam- age and pain to the central nervous system. Substance P is released by small-diameter, unmy- elinated axons (C-fibers) in the substantia gelatinosa and excites neurons whose axons carry information about pain to the brain (Figure 7.4). However, centers in the cerebrum and brain stem project axons down to the substantia gelatinosa. These axons release endorphins that alter the pain information that actually reaches the cerebrum (Watkins & Mayer, 1982).
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CHAPTER 7Section 7.2 Somatosensory Processing
Figure 7.4: The Gate-Control Theory of Pain: Ascending and descending pain systems
Figure A: If the “gate” in the substantia gelatinosa is open, information about pain (traveling in C-fibers) is sent to the cerebrum, and pain reaches consciousness. Figure B: In the substantia gelatinosa, C-fibers release substance P, which activates a pain signal that is sent to the cerebrum. Endorphin-producing neurons in the brain stem have axons that terminate on the C-fibers in the substantia gelatinosa and inhibit the release of substance P.
You first learned about the endogenous opiate neurotransmitters, called endorphins, in Chapter 3. Input from higher brain centers causes neurons in the brain stem to release endorphins at their terminal buttons in the substantia gelatinosa (Figure 7.4). The release of endorphins in the substantia gelatinosa stops the pain signal generated by substance P (Beaudry, Dubois, & Gendron, 2011).
What causes a football player to be able to play to the end of a game after breaking a rib? We’ve all heard stories of people with horrible injuries who are somehow able to ignore pain and finish the task at hand. The explanation is found in Melzack and Wall’s Gate-Control Theory. Higher brain centers send input via brain stem areas that blocks pain messages coming from the receptors. If a person switches his or her attention to winning the game or rescuing a loved one, pain messages can be suppressed by endorphins, which are released in response to signals from higher brain centers that control attention and motivation.
Treatment for Pain Many treatments for pain can be explained by the Gate-Control Theory. Most pain treatments produce analgesia, which is the absence of pain without loss of consciousness. Thus, analgesics are drugs that reduce the experience of pain. The “For Further Thought” box describes the action of various drugs, including some new experimental substances, used to treat pain.
A. B.
Brain (central control)
Spinal cord
Final output of gate system: “pain”
A-fibers
Input stimulation
C-fibers
Gate-control system
Substantia gelatinosa
Axon carrying pain information to brain
Receiving neuron (in substantia gelatinosa)
Substance P receptors
Substance P
C-fiber Primary sensory neuron
Endorphin
Endorphin receptors
Periaqueductal gray neuron
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CHAPTER 7Section 7.2 Somatosensory Processing
For Further Thought: Pharmacological Treatments for Pain
The term pharmacological (which has the same root as phar- macy) refers to the action of drugs. Drugs have been used to treat pain for thousands of years, but our understanding of the biological mechanisms underlying such pharmacological treat- ments has just begun. As investigators discover how particular painkillers work, we are learning that pain control is indeed a very complicated process in the nervous system.
Drugs that treat pain are typically classified into one of two categories: opiate or nonopiate drugs. Regardless of their classification, all painkilling drugs vary in their effectiveness in treating different kinds of pain. Aspirin, for example, is not effective in blocking postoperative pain, whereas opiates are not very effective in inhibiting pain associated with movement (MacPherson, 2000). On the other hand, aspirin is quite effec- tive in reducing pain associated with movement, and opiates are used routinely after surgery to control pain.
Opiate drugs, as you learned in Chapter 3, are chemically simi- lar to opium, which is derived from the poppy plant. The best- known opiates that are used to treat pain are morphine, Demerol, Darvon, codeine, OxyContin (oxyco- done), and Percodan. A wide variety of techniques are used to administer opiate medication, including oral, rectal, intravenous, transdermal (through the skin), inhalation, and epidural (into the meninges of the spinal cord) administration. Adverse side effects of opiate painkillers include difficulty breathing (producing death in drug overdoses), nausea, and other types of gastrointestinal upset.
Nonopiate analgesics treat pain in many different ways. Over-the-counter analgesics such as aspirin, acetaminophen, and ibuprofen block the production of prostaglandins, chemicals that are released when body tissue is damaged and cause pain, fever, and inflammation (Garavito, 1999). Anticonvul- sants (drugs that stop seizures) inhibit pain by blocking Na+ channels. Certain antidepressants also have analgesic effects, but they work by blocking reuptake of norepinephrine and serotonin. Tramadol is an interesting drug because it blocks pain by binding with the mu-opioid receptor and by inhibiting reuptake of norepinephrine and serotonin. Other classes of nonopiate painkillers include drugs that bind with adrenergic receptors (for example, clonidine) and drugs that antagonize glutamate receptors (for example, ketamine).
A number of drugs are currently being tested in clinical trials in humans for their safety and effective- ness in treating pain (McGivern, 2007; Rainsford, 2007). Epibatidine is an alkaloid derived from the skin of a poisonous frog and has been demonstrated to produce analgesia in rats. Studies have shown that epibatidine stimulates nicotinic acetylcholine receptors. Likewise, a toxin from snails also has been shown to reduce pain, as have essential oils from various plants (Campêlo et al., 2011; Mendes et al., 2010). Another new analgesic drug currently under investigation, called nitroaspirin, is a combi- nation of aspirin and the neurotransmitter nitric oxide (Herrero, Romero-Sandoval, Gaitan, & Mazario, 2003). Clinical trials are also underway to test in carefully controlled studies the effectiveness of can- nabinoids (marijuana-like neurotransmitters) in treating pain (Lal et al., 2011).
iStockphoto/Thinkstock
Photo 7.1 Aspirin is a pharma- cological treatment for pain but is not an opiate derivative.
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CHAPTER 7Section 7.2 Somatosensory Processing
Nonpharmacological methods for treating pain include counterirritation, acupuncture, and transcutaneous electrical nerve stimulation. Counterirritation involves using a brief irritating stimulus to counteract ongoing pain. It is a technique that has been used for centuries to alleviate pain. Acupuncture is a pain control method developed by Chinese doctors more than 4,000 years ago. In some ways acupuncture works like counterir- ritation. Thin needles are inserted into the skin at spe- cial points, often far from the site of pain, and vibrated slightly. For example, to alleviate tooth pain, Mayer (1975) stimulated acupuncture points in the subjects’ hands. Another form of counterirritation is transcuta- neous electrical nerve stimulation (abbreviated TENS). This technique involves sending a tiny current to the skin to stimulate receptors in the area of the injury to induce analgesia (Carroll et al., 2001). Often, people who are receiving TENS will wear a little box clipped to a belt, with wires extending from the box to the site of stimulation. These three forms of treatment— counterirritation, acupuncture, and TENS—appear to
activate both the endorphin and the nonopiate pain-inhibitory systems (Asher et al., 2010; Nigam, Taylor, & Valeyeva, 2011; Watkins & Mayer, 1982).
Cortical Processing of Pain Information about all body sensations, including pain, first goes to the primary somatosensory cortex upon reaching the cerebrum. Next, information about pain is relayed to the secondary somatosensory cortex (the somatosensory “What” and “Where” regions) in the parietal lobe. From these areas in the parietal lobe, pain information is sent to the frontal lobe for processing of the emotional and qualitative components of pain, which permits us to evaluate the source and seriousness of the pain and plan our reaction to it (Stuss & Knight, 2012).
Evaluation of the emotional dimension of pain, such as its unpleasantness and whether it can be endured, appears to involve the anterior cingulate cortex in the frontal lobe. Patients with prefrontal lobotomies that destroyed the cingulate cortex can still feel pain, but they do not find it unpleasant or distressing (Rainville, Hofbauer, Bushnell, Duncan, & Price, 2000). With PET imag- ing, Bud Craig and his colleagues (1996) found that the anterior cingulate cortex becomes active when subjects touch painfully hot or cold stimuli but remains inactive when the same subjects touch warm or cool stimuli.
It is important to remember that the cerebral cortex communicates with subcortical structures such as the hippocampus, the hypothalamus, and brain stem areas about the presence and quality of pain (Hsieh, Stahle-Baeckdahl, Haeermark, & Stone-Elander, 1996). The hippocampus processes this information, laying down memories of the painful stimulus, which will influence subsequent emotional reactions to the stimulus. The hypothalamus contributes to the inhibition of pain by stimulating the pituitary gland to release endorphins. As you learned earlier in this section, stimulation of pain-related brain stem areas causes neurons in these areas to release endorphins and other nonopiate neurotransmitters that inhibit pain.
Creatas/Thinkstock
Photo 7.2 Acupuncture is a pain control method that works like counterirritation.
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CHAPTER 7Section 7.2 Somatosensory Processing
A PET study by Jon-Kar Zubieta and his colleagues (2001) at the University of Michigan has demonstrated that sustained jaw pain produced in healthy human subjects triggers the release of endogenous opioids in a number of cortical and subcortical brain regions, including the anterior cingulate cortex, prefrontal cortex, thalamus, hypothalamus, and amygdala. As mu- opioid receptor activity increased, the participants reduced their subjective ratings of the pain experience. Thus, pain that is experimentally induced in the laboratory activates the release of endorphins in cortical and subcortical areas associated with sensory, emotional, and cognitive dimensions of pain.
In summary, the experience of pain results from the activation of pain receptors in the periph- eral nervous system and the responses of cortical and subcortical structures in the brain to that activation. In people who have experienced devastating tissue injury, the central nervous system can continue to issue pain responses in the absence of stimulation from the peripheral nervous system, as is the case with phantom limb pain. Additionally, reorganization of the somatosensory cortex can cause a mix-up in the processing of signals reaching the brain. For example, allodynia is an abnormal pain response to a normally nonpainful stimulus that is observed in individuals who have suffered tissue and nerve damage. A light touch on the skin can produce horrible pain in patients with allodynia. The brains of these patients come to interpret many nonpain messages as painful, which activates the emotional and cognitive centers to respond to the nonpainful stimu- lus as if it were a source of excruciating pain.
As we conclude this discussion of pain perception, please keep in mind that scientists are still investigating precisely how pain is processed in the central nervous system. Investigators who study pain have not reached a consensus concerning the role of the cerebral cortex in the percep- tion of pain. We know even less about the mechanisms of smell perception and taste perception in the brain—topics that we will examine next in this chapter.
Disorders of the Somatosensory System
Because of the diverse nature of the somatosensory system, the disorders of this sensory system take many forms. For example, viral infections can interfere with signals coming from the stretch receptors of the proprioceptive system, which will leave the patient without a body image. When carrying an object, one patient had to watch her hands constantly (Sacks, 1985). Otherwise, she would not be aware of the object in her hands, and she would drop whatever she was holding. Another patient would stumble and fall in dark rooms because he could not walk if he couldn’t see his feet (Cole, 1995).
One rare but extremely interesting disorder (called congenital insensitivity to pain) occurs in people born without pain receptors (Cox et al., 2006). These individuals retain all of their other somatosensations, but they cannot feel pain. As children, they require constant supervision and care because they get no clues from their environment as to what is dangerous. For example, extremely hot food can burn their mouths, and they must be taught to blow on their food to cool it down. When pain insensitivity is accompanied by mental retardation, patients often mutilate themselves because they cannot feel the pain and do not understand the consequences of body injury (Berkovitch, Copelimitch, Tauber, Vaknin, & Lahat, 1998).
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CHAPTER 7Section 7.3 The Olfactory System
7.3 The Olfactory System
Our sense of smell, or olfaction, provides us with a tremendous amount of information about our environment. Most other animals rely on their sense of smell for survival: for finding mates, locating food, and avoiding predators. In contrast, humans tend to rely on their eyes and ears more than on their noses for information about the world around them. But imagine how you would learn to know the world if you could not see or hear. Helen Keller used her sense of smell to identify objects around her. For example, she could distinguish a wide variety of flowers by their smell, as she described in the book she wrote about her life:
I used to feel along the square stiff boxwood hedges, and, guided by the sense of smell, would find the first violets and lilies. . . . Here, also, were trailing clematis, drooping jasmine, and some rare sweet flowers called butterfly lilies. . . . But the roses—they were loveliest of all. (Keller, 1954, pp. 24–25)
You might assume, as many people do, that deaf or blind people have a much better sense of smell than people with normal hearing or vision. Research comparing the olfactory ability of blind human subjects with sighted subjects has demonstrated that blind subjects are not significantly better than sighted subjects in odor detection or odor discrimination (Smith, Doty, Burlingame, & McKeown, 1993). In fact, sighted subjects who were employed as water quality evaluators did far better than blind and untrained sighted subjects on tests of taste and smell ability. Helen Keller and others with visual or auditory impairments had to learn to use their sense of smell to obtain information about the world around them.
Although we humans don’t depend on our noses to find food or mates, our sense of smell is quite acute. Most people can recognize about 10,000 odors and can detect a drop of perfume that evaporates in a room the size of a large classroom. Human subjects have demonstrated that they can correctly sort T-shirts into two piles—those that have been worn by men and those that have been worn by women—based on their smell alone (Lord & Kasprzak, 1989; Schleidt, Hold, & Attili, 1981). Even very young human infants, just a few weeks old, can identify the scent of their own mothers, preferring T-shirts worn by their mothers to T-shirts worn by other lactating women (Russell, 1976). There is also evidence that men and women can differentiate among human vagi- nal odors associated with ovulation and premenstrual vaginal odors (Doty, 1997; Doty, Ford, Preti, & Huggins, 1975; Haselton & Gildersleeve, 2011).
The Nature of Odors
Odors are produced by chemicals that are dissolved in the air. That is, in order for a chemical to have a smell, it must be volatile, which means it must be gaseous at room temperature. However, not all chemicals dissolved in the air have an odor. For example, water vapor has no smell. In gen- eral, substances that contain carbon (organic substances) have an odor, although not all organic matter has an odor. Molecules that have an odor are called odorants.
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CHAPTER 7Section 7.3 The Olfactory System
Anatomy and Function of the Olfactory System
Olfactory receptors are neurons that respond to chemicals associated with particular odors. Because they are bipolar neurons, each olfactory receptor has an axon and one dendrite (Figure 7.5). At the end of each dendrite is a dendritic knob from which many fine hair-like projections, called cilia, extend. These cilia have receptor sites that bind with specific chemicals. When an air- borne chemical binds with a receptor site on a cilia, an action potential is initiated, which causes neurotransmitters to be released at the axon terminal. Thus, olfactory receptors use neurotrans- mitters to signal to the brain that an odor is present.
Figure 7.5: Olfactory receptors
The olfactory receptor is a bipolar neuron with a dendritic knob located at the end of the dendrite. Cilia on the dendritic knob contain receptor sites for odorants.
Olfactory receptors are located in the olfactory epithelium at the top of the nasal cavity. The human nose contains approximately 10 million olfactory receptors on each side. Dogs have 10 times more receptors than humans do. They also have more cilia and thus more receptor sites per olfactory receptor, which contributes to their superior sense of smell. For example, bloodhounds need only a few molecules of an odorant to detect an odor. When tracking a scent, bloodhounds are able to follow a scent to a riverbank, swim across the river, and pick up the scent on the other bank.
Cilia
Olfactory neurons
Nucleus of cell
Basal cell (precursor to
olfactory neuron)
Dendrite
Dendritic knob
Odorant
Cilia
Olfactory neurons
Nucleus of cell
Basal cell (precursor to
olfactory neuron)
Axon to olfactory bulb
Dendrite
Dendritic knob
Nasal cavity
Odorant
Lining of nasal
cavity
Mucous layer
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CHAPTER 7Section 7.3 The Olfactory System
Also located in the olfactory epithelium is another type of cell, called a neuronal stem cell. Neu- ronal stem cells give rise to new neurons. You learned in Chapter 2 that neurons are not usually replaced when they die. However, olfactory sensory neurons die and are sloughed off with the outer layers of the olfactory epithelium about once a month. New olfactory receptors are gener- ated by the stem cells to replace the dead cells.
On the surface of each cilia of the olfactory sensory neuron are special proteins that act as binding sites for odorants. The receptor sites on olfactory sensory neurons are G protein-coupled recep- tors, which you learned about in Chapter 3. Each protein receptor site binds with one and only one chemical. John Amoore (1971) has proposed the Stereochemical Theory of Odor to explain how specific odorants excite olfactory sensory neurons. According to the Stereochemical Theory, each odorant is a chemical substance that has a particular shape, and each shape fits into the receptor site like a key fits into a lock. That is, when a molecule has the correct shape, it fits precisely into the binding site, which produces a depolarization that generates an action potential in the olfac- tory neuron. This theory is considered too simplistic today, but its general concept of a molecule fitting into a specific receptor site is correct.
If we can recognize 10,000 different odors, how do neurons code for each of these smells? Research by Richard Axel (1995) and his colleagues has demonstrated that each olfactory sen- sory neuron contains only one type of receptor site on its cilia. Altogether, according to Axel’s research, we have 1,000 different receptor proteins, which means that we have 1,000 different types of olfactory sensory neurons. In order to detect 10,000 different odors, odorants must bind with more than one type of receptor protein. For example, the odorant vanillin, which produces a vanilla odor, has a number of functional units that are capable of binding with various receptor sites on different neurons. Groups of sensory neurons forward axon potentials to the brain, with different groups of neurons being activated for different smells (Yoshihara, Nagao, & Mori, 2001).
Approximately 10 million axons, from each side of the nose, leave the olfactory epithelium and pass through the skull to form the olfactory nerve, or cranial nerve I (Figure 7.6). The skull bone in this region is called the cribiform plate. It is very porous, due to the millions of holes that allow the olfactory axons to exit the nasal cavity from the nose to the brain, and thus is quite weak. For example, any object that can pass through the nostril, such as a pencil, can very easily shatter the cribiform plate and enter the brain.
The olfactory nerve goes directly to the olfactory bulb, which is situated between the cribi- form plate and the frontal lobe (Figure 7.6). Axons coming from the olfactory sensory neurons, which make up the olfactory nerve, separate and individually project to special structures, called glomeruli, in the olfactory bulb. Each neuron sends its axon to only one glomerulus. Axel (1995) and his colleagues have demonstrated convincingly that each glomerulus receives information from neurons that bear the same type of receptor protein. That is, each glomerulus processes information about only one kind of odor (Yoshihara et al., 2001).
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CHAPTER 7Section 7.3 The Olfactory System
Figure 7.6: Anatomy of the olfactory system
Odor molecules bind with receptors on the cilia of olfactory receptors located on the roof of the nasal cavity. The axons of the receptors form cranial nerve I as they pass through the skull to the olfactory bulb.
The olfactory bulb sends the information about odors to the cerebrum and to structures in the limbic system, such as the hippocampus and the amygdala. Information about smell is sent to two different areas in the cerebral cortex: to the olfactory cortex in the temporal lobe and to the pre- frontal cortex, where the odor is consciously detected and identified.
An Accessory Olfactory System
Like other animals, humans appear to have two olfactory systems (Bartoshuk & Beauchamp, 1994; Takami et al., 1993). The primary olfactory system, which you’ve just learned about, allows us to detect and recognize odors. The second system, called the accessory olfactory system, transmits information about pheromones, the chemical signals that regulate sexual and social behaviors. In many species, including rodents and farm livestock, pheromones released by the female of the species signal that she is available for mating, which initiates sexual behavior in the male (Wysocki & Meredith, 1987). In humans the role of pheromones and the accessory olfactory system is much less important in controlling or initiating behavior (Miller & Maner, 2011).
Sensory neurons for the accessory olfactory system are located in the vomeronasal organ in the floor of the nasal cavity (Figure 7.6). When the neurons in the vomeronasal organ are stimulated by pheromones, action potentials race down their axons to signal to neurons in the hypothala- mus and other areas of the brain stem. Information from the accessory olfactory system is not processed by the olfactory bulb and, therefore, does not reach the cerebrum, where conscious processing of odors occurs.
Air in
Nasal cavity
Olfactory bulb
BrainBrain
Skull
Olfactory nerve (cranial nerve I) passes through skull
Olfactory epithelium Olfactory epithelium
Vomeronasal organ
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CHAPTER 7Section 7.3 The Olfactory System
Thus, processing of olfactory information in the accessory olfactory system is largely unconscious. That is, we are generally unaware when olfactory receptors in our vomeronasal organ are stimu- lated. For example, women who live together tend to menstruate at the same time (McClintock, 1971; Preti, Cutler, Garcia, Huggins, & Lawler, 1986). Investigators believe this menstrual synchrony occurs because the women exchange chemical signals by way of the accessory olfactory system. In addition, women who live with men tend to have shorter, more regular menstrual cycles. Chemi- cals in men’s sweat have been shown to affect women’s menstrual cycles (Cutler, Preti, Krieger, & Huggins, 1986).
Olfactory Processing
Natural odors consist of many different molecules mixed together. The task of the olfactory system is to sort out these various chemicals and to identify the odor present at any given time. When you consider all the thousands of volatile chemicals that can possibly stimulate the olfactory recep- tors, the job of the olfactory system seems impossibly hard.
On the other hand, the olfactory system is remarkably simple, compared to the visual, auditory, or somatosensory systems. The olfactory processing center in the cerebral cortex is only two syn- apses away from the receptors. In addition, the olfactory system does not appear to separate into functional streams, like the “What” and “Where” streams of the other perceptual systems that we’ve studied (Laurent, 1999).
Research at Stanford University has identified the location of the primary olfactory cortex and the secondary olfactory cortex in humans. Using functional MRI, Sobel and his colleagues (1998) discovered that when a person sniffs, an area of the temporal lobe is activated (Figure 7.7). That is, the primary olfactory cortex in people is located in the temporal lobe. When a human subject becomes aware of an odor, the secondary olfactory cortex is activated. The secondary olfactory cortex is found in the orbitofrontal prefrontal cortex, an area of the frontal lobe directly behind the eyeball socket in the skull (Sobel et al., 1998).
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CHAPTER 7Section 7.3 The Olfactory System
Figure 7.7: The primary and secondary olfactory centers
The primary olfactory cortex is located in the piriform cortex in the temporal lobe. The secondary olfac- tory cortex is found in the orbitofrontal prefrontal cortex.
From “Long-Term Change of Mind” by Michael Merzenich. In Science 6 November 1998: Vol. 282 no. 5391 pp. 1062–1063. Reprinted with permission from AAAS.
Gender Differences in Olfactory Ability In tests of odor detection and odor identification, women consistently outperform men. This supe- riority in olfactory ability in women has been demonstrated in Black American, White American, Korean American, and native Japanese subjects (Doty, Applebaum, Zusho, & Settle, 1985; Doty & Cameron, 2009). These findings have been reproduced in brain-recording and brain-imaging stud- ies. For example, women are more susceptible to olfactory stimuli than men (Evans, Cui, & Starr, 1995). David Yousem and his colleagues (1999) presented a variety of pleasant and unpleasant odors to eight men and eight women while their brains were being scanned, using functional MRI. The images of the women’s brains showed up to eight times more activation in the frontal lobes than those of the men when they received olfactory stimulation. In both men and women, the right frontal lobes showed more activation associated with olfaction than did the left. However, for both the left and right frontal lobes, the level of activation in response to odors is greater in women than in men.
Occipital lobe
Orbitofrontal prefrontal cortex (secondary olfactory cortex)
Primary olfactory cortex Piriform
cortex
Temporal lobe
Parietal lobeFrontal
lobe
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CHAPTER 7Section 7.3 The Olfactory System
Case Study: A Case of Anosmia
Chris was a senior in high school when he had what he considers to be the worst case of flu he’s ever had in his life. He had the usual sore throat, headache, fatigue, and nasal conges- tion that one would expect with a bad viral infection, and he also found that his food lost its flavor, which he blamed on his stuffy nose. However, when his flu symptoms went away, his sense of taste was still disturbed. What’s more, Chris had developed anosmia—an inability to detect odors.
After several weeks, when his sense of smell did not recover, Chris’s parents took him to his family doctor, who assured him that his olfac- tory sense would return. He waited more than a month and, in the meantime, lost a good deal of weight (nearly 40 pounds) because he no longer liked to eat. Eating had become a chore because he could not smell the food on his plate, and the food itself seemed to have no flavor.
He went next to a series of specialists when his olfactory sense did not return after 6 weeks. The spe- cialists ordered CAT scans, examined his nasal cavity using tiny cameras, and took biopsies from his oral and nasal pharynx (pharynx means “throat” in Greek). The results of all these tests were inconclusive. One specialist noted a good deal of scar tissue in the nasal cavity and suggested that, when the scar tissue shrank, Chris’s sense of smell would return.
About 5 months after the onset of anosmia, Chris’s olfactory sense began to recover. At first, he was bothered by phantom odors that would occur randomly during the day. For example, he was sitting in class one day when he suddenly smelled the swimming pool where he had worked as a lifeguard the summer before. As Chris approached complete recovery, other strange odors began to haunt him more frequently. Chris’s sense of smell returned to normal about 7 months after he first developed anosmia.
Sky View/Photodisc/Thinkstock
Photo 7.3 Anosmia is the inability to smell odors. Depending on the cause, it can be temporary or permanent.
Disorders of the Olfactory System
The olfactory disorder that has received the most study is anosmia, which is an inability to smell. Some people have total anosmia and cannot detect any odors whatsoever. For example, individu- als with a genetic disorder known as Kallmann syndrome lack an olfactory system. In addition, viral infections that invade the olfactory system can produce temporary or permanent anosmia, as described in the “Case Study.” In fact, any condition that blocks the nasal cavity or damages the olfactory system can produce anosmia, including sinus disease, nasal tumors or polyps, head injury, and upper respiratory infections such as the common cold that induce the production of large quantities of mucus that block the nasal passages.
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CHAPTER 7Section 7.4 The Taste System
7.4 The Taste System
Your sense of taste provides you with information about the foods you are ingesting. Sweet-tasting substances are generally a ready source of calories, whereas poisons and spoiled foods typically have a bitter taste. Human breast milk, for example, is an excellent source of nutrition and is sweet-tasting. For that rea- son, we usually react positively to sweet-tasting substances and neg- atively to bitter-tasting substances. Studies of very young infants have demonstrated that reactions to dif- ferent tastes appear to be innate. Babies offered sweet-tasting food will appear to smile and move toward the food source. When a bitter-tasting substance is placed on a baby’s tongue, the baby screws up its face in disgust and pulls away from the experimenter.
The Nature of Taste Stimuli
Taste stimuli are chemicals that are dissolved in water. Saliva, which is mostly water, dissolves solid food particles, permitting them to interact with taste receptors. If dry salt or sugar is sprinkled on the surface of a dry tongue, the salt or sugar crystals will have no taste because the crystals are incapable of stimulating taste receptors in their dry, undissolved state. But if salt or sugar is sprinkled on a wet tongue, the crystals will dissolve in the saliva on the tongue and stimulate taste receptors, producing a salty or sweet taste.
In the previous section on the sense of smell, you learned that people possess about 1,000 differ- ent olfactory receptors that respond to at least 10,000 different odors. The taste system, on the other hand, limits people to five primary tastes: sweet, sour, salty, bitter, and umami. Umami, the taste that characterizes Asian foods, is an identified primary taste in which people respond to the taste of glutamate. Umami has its own specific receptors on the tongue and a special processing area in the cerebral cortex (Rolls, 2000).
Sour tastes are produced by substances that are acidic. A wide range of substances produces a sweet or bitter taste, and the receptor mechanisms for these primary tastes are still being debated. Most substances that taste sweet or bitter are organic substances, such as sugars or amino acids, that contain carbon. However, some metals (for example, lead), which contain no carbon, have a sweet taste. Lead poisoning occurs in children who are attracted to the sweet taste of peeling lead paint or other lead-based products and eat significant quantities of these substances.
Stimulation of a taste receptor by one food can produce adaptation in that receptor, which will alter the taste of other foods that are introduced to the mouth after adaptation has taken place. For example, if you eat a piece of chocolate fudge cake with chocolate icing and then drink a sip
Polka Dot Images/Polka Dot/Thinkstock
Photo 7.4 Our reaction to different tastes is an innate quality.
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CHAPTER 7Section 7.4 The Taste System
of cola, the cola will taste bitter and not sweet. This is because the chocolate cake will stimulate sweet receptors intensely, producing adaptation of those receptors. Therefore, when the cola is introduced to the sweet receptors, they do not respond. Only the bitter and salty receptors respond because cola has a weak bitter and salty taste, as well as a powerful sweet taste.
Another phenomenon, called potentiation, also occurs in taste receptors. With potentiation, one taste stimulus causes a receptor to respond more intensely to another stimulus. Have you ever drunk orange juice after brushing your teeth? Ugh, what an awful taste! This is a great example of potentiation. The detergent in the toothpaste alters the bitter receptors on your tongue, increas- ing their ability to respond. So, when you drink orange juice immediately after brushing your teeth, the bitter receptors in your mouth increase their activity, producing a sensation of bitter- ness when stimulated by orange juice.
Flavor is a sensory quality that combines olfaction and taste. When you have a bad cold that clogs up your nasal passages, making it impossible for odorants to come in contact with olfactory recep- tors, the flavors of the food you eat are distorted. That is, stimulation of the taste receptors alone does not elicit the complete sensation of flavor.
Anatomy and Function of the Taste System
Like the olfactory system, the taste (or gustatory) system contains chemoreceptors. Unlike olfac- tory receptors, taste receptors do not have dendrites or axons. Taste receptors have tiny finger- like processes, called microvilli, that project into the mouth, where they come into contact with chemicals that act as taste stimuli. The taste stimuli cause changes in the receptor membrane, either opening sodium channels or closing potassium channels, which depolarizes the receptor cell. Information about this depolarization is sent to the brain by way of neurons that communi- cate with the receptor cells.
The chemoreceptors of the taste system, called taste receptors, are embedded in the linings of the mouth and throat. However, most taste receptors are found on the tongue in structures known as taste buds. Taste buds are located on the surface of the little bumps, called papillae (the singular is papilla), that cover the tongue. The taste receptors have little hair-like projections, or microvilli, that protrude through pores in the surface of the tongue. When taste stimuli come in contact with these microvilli, they initiate a receptor potential, which excites neurons that send information about taste stimuli to the brain.
Information about the intense burning produced by spicy or “hot” foods is transmitted to the brain by way of cranial nerve V, the trigeminal nerve.
Taste Processing
Investigators are just beginning to understand the mechanisms by which taste is processed in the cerebral cortex. As you have just learned, information from taste receptors reaches the brain by way of three cranial nerves, which synapse with neurons in the nucleus of the solitary tract. From the hindbrain, information about taste is transmitted to the thalamus and then on to the primary taste cortex, in the most inferior aspect of the frontal lobe, adjacent to the temporal lobe, called the insula. Bornstein (1940) studied a dozen men with bullet wounds in the primary taste cortex (Figure 7.8). Bornstein’s subjects all exhibited taste impairments.
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CHAPTER 7Section 7.4 The Taste System
Since Bornstein’s original research, a number of lesioning experiments in monkeys and recording studies in human and monkey subjects have verified that the primary taste cortex in primates is located in the insula. Damage to the insula will impair taste perception, as Bornstein first noted in 1940. Patients with lesions in the primary taste cortex demonstrate both a loss of taste sensitiv- ity and an inability to recognize previously familiar tastes (Pritchard, Macaluso, & Eslinger, 1999).
Figure 7.8: The primary taste cortex
The primary taste cortex is located in the insula, which is in the frontal lobe.
The role of the insula in taste perception is unknown, although studies of brain-damaged indi- viduals indicate that it plays a role in the conscious processing and identification of specific tastes (Nunn, Frampton, Fuglset, Törzsök-Sonnevend, & Lask, 2011; Veldhuizen, Douglas, Aschenbrenner, Gitelman, & Small, 2011). However, identification of tastes also appears to occur in the brain stem, as studies of lesioned rats and human infants born without a cerebrum (called anencephalic infants) have shown. Anencephalic babies show the same reaction as do babies with intact brains when exposed to different tastes (Steiner, 1977). When a sweet taste is placed on their tongues, anencephalic and normal infants make a pleased expression and move toward the food source. Like normal babies, anencephalic babies screw up their faces in disgust when offered a bitter- tasting substance.
Occipital lobe
Insula (primary taste cortex)
Temporal lobe
Parietal lobeFrontal
lobe
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CHAPTER 7Section 7.5 The Vestibular System
Disorders of the Taste System
Ageusia is the inability to taste. Rarely do people have total ageusia, which is a complete absence of the ability to taste. However, a few genetic disorders do produce total ageusia, and head trauma and viral infections can produce temporary total ageusia. Most forms of ageusia are specific ageusias in which an individual cannot sense a particular taste or family of tastes. One well-researched example is the substance phenylthiocarbamide, or PTC, which produces a bitter taste in people who have inherited the ability to taste this chemical. About 25% of all Americans cannot taste PTC, although they can taste other bitter substances (Bartoshuk, Duffy, & Miller, 1994; Guo & Reed, 2001).
Perhaps the most disturbing taste disorder for any individual is dysgeusia, in which the individual has a disagreeable taste in the mouth that is due to a nose, mouth, or throat infection, medication, or chemotherapy (Hovan et al., 2010). Sometimes the dysgeusia is due to “phantoms” caused by damage to the taste system. In the case of taste phantoms, there are no physical stimuli in the month that elicit the dysgeusia. Rather, irritation of the peripheral or central nervous system produces the sensation of a bad taste in the mouth. For example, El-Deiry and McCabe (1990) reported the case of a 54-year-old man with a tumor in his temporal lobe that caused a phantom foul, bitter taste in his mouth.
7.5 The Vestibular System
When he was much younger, my youngest son loved to spin around in circles. Arms out-stretched, he would go around and around. Then he would stop abruptly and wait for that dizzy feeling, that sensation that the world was still spinning even though he was not. This spin- ning sensation arises from the vestibular system. Usually you are not aware when your vestibular system is working. But when something is wrong, like when your eyes and vestibular system send contradictory messages to the brain, you become consciously aware of the vestibular system. In this section we will examine this sensory system that you largely take for granted.
The vestibular system shares many similarities with the auditory system. Like the auditory system, the vestibular system is located in the temporal bone in the same cavity as the inner ear. A bony maze comprising the vestibular system is located deep within the temporal bone. The vestibular receptors are mechanoreceptors called hair cells, identical in appearance to those in the auditory system. In addition, information from the vestibular hair cells is forwarded to the brain by way of the vestibular branch of the auditory nerve, cranial nerve VIII.
The Nature of Vestibular Stimuli
The main function of the vestibular system is to detect changes in head movement in order to assist the eyes in vision. Your eyes are like two cameras mounted on a moving tripod. Have you ever seen a video that was filmed while the video camera was bouncing around? This is a popular technique in action-adventure movies such as the Bourne films or Cloverfield. That’s what the image that is sent to your brain looks like. But the vestibular system informs your brain of head movements, and the visual system compensates for these movements, the net result being a visual image that appears clear and stable. Therefore, any changes in head movement, such as
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CHAPTER 7Section 7.5 The Vestibular System
speeding up or slowing down or turning the head, act as stimuli that excite vestibular receptors. Static head positions (that is, head positions that do not change) are also registered by certain receptors in the vestibular system. These receptors are particularly sensitive to the position of the head with respect to gravity.
Anatomy and Function of the Vestibular System
The hair cells are located in three organs that make up the vestibular system: the utricle, the sac- cule, and the semicircular canals. You have one utricle, one saccule, and three semicircular canals on either side of your head (Figure 7.9). In the utricle and saccule, the hair cells are found in a sensitive area. The hair cells in the utricle get stimulated when the head is upright. In contrast, when the head is in a horizontal position, the hair cells of the saccule are maximally stimulated. For example, when you are lying in bed or lying on the sofa watching television, the hair cells in your saccule fire wildly.
Figure 7.9: Anatomy of the vestibular system
The vestibular system’s intricate parts all work together to detect any changes in your head’s movement to assist in your eyes’ adjustment to altered vision.
The primary function of the hair cells in the utricle and saccule is to gather information about the position of the head with respect to gravity. They are our gravity detectors. In contrast, the hair cells in the semicircular canals relay information about head movement.
There are three semicircular canals, oriented at 908 to each other, on each side of the head (Figure 7.9). At the ends of each of the canals are swellings, where the hair cells are located. The hair cells are found in cristae (the singular is crista) located in the ends of the canals. Each crista contains a cluster of hair cells covered by a mass of jelly-like substance. Movement of the head causes fluid in the semicircular canals to move. As the fluid in the semicircular canals moves, it causes shaking of the jellied mass, which tugs and pulls at the hairs of the hair cells, producing action potentials.
Cochlea
Saccule
Ampulla
Vestibular branch of auditory nerve
Utricle
Semicircular canal
Otoliths Hair Cells
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CHAPTER 7Section 7.5 The Vestibular System
Brain Pathways Carrying Vestibular Information
Action potentials produced by cells in the utricle, saccule, and semicircular canals are relayed to the brain by way of cranial nerve VIII, the auditory nerve. As you have already learned, the audi- tory nerve enters the brain at the level of the medulla. The vestibular branch of the auditory nerve goes to the vestibular nucleus. From the vestibular nucleus, axons carrying information from the vestibular system travel in bundles to various regions of the central nervous system.
Recall that the vestibular system’s main function is to assist with vision. Movement of the head causes compensatory movement of the eyes. Look at yourself in the mirror, keeping your eyes on your eyes in the mirror. Move your head to the left, and you’ll observe that your eyes will move to the right. When you fix your gaze on an object, your vestibular system works with the nerves that control your eye muscles, so that you keep your eyes on the object as you move your head. These automatic eye movements that are made in response to head movements are called ocu- lovestibular reflexes.
Nystagmus is another example of an oculovestibular reflex. Continuous stimulation of the vestibu- lar system (for example, the stimulation produced by spinning in circles) induces nystagmus, or oscillation of the eyes, in which an individual’s eyes move laterally a short distance before jumping back to their original position and then start to move laterally again. The eyes move in response to messages being sent to the brain by the semicircular canals. These messages inform the brain that the head is moving, and the neurons controlling eye movement produce compensatory move- ments of the eyes.
Some axons from the vestibular nucleus travel to the cerebellum and reticular formation, whereas others travel to the spinal cord, via the vestibulospinal tract, which goes from the vestibular nucleus to the spinal cord (Figure 7.10). The vestibular system transmits and coordinates informa- tion that helps us maintain an upright posture with respect to gravity and maintain balance (High- stein & Holstein, 2012). For example, the righting reflex permits us to recover our upright posture when we stumble or fall over.
In addition, a number of axons coming from the vestibular nucleus synapse with neurons associ- ated with cranial nerve X, the vagus nerve. Recall that the vagus nerve innervates structures in our upper abdomen, chest, and neck, including the stomach. Overstimulation of the vestibular system produces motion sickness, with which an individual feels nauseous and may even vomit. For example, a roller-coaster ride may trigger vomiting because stimulation of the vestibular system triggers the vagus nerve, which stimulates the stomach to eject its contents. For some people, even mild stimulation of the vestibular system, such as a car ride or jet flight, produces motion sickness.
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CHAPTER 7Section 7.5 The Vestibular System
Figure 7.10: Vestibular pathways
From the vestibular nuclei, axons carry vestibular information to the cerebellum, the cranial nerve nuclei, and finally the vagus nerve.
Finally, some axons leaving the vestibular nucleus send their information to the cerebral cortex. This information first goes to the thalamus and then on to the vestibular sensory cortex in the temporal lobe. When this information reaches the cerebral cortex, we become consciously aware of vestibular stimulation.
Direction of movement of eyes
Nucleus of cranial nerve III
Nucleus of cranial nerve VI
(To and from cerebellum)
Vestibular nerve
Horizontal semicircular canal (direction of flow of endolymph)
Vestibulospinal tract
Vagus nerve (cranial nerve X)
Vestibular nuclei
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CHAPTER 7Section 7.5 The Vestibular System
Disorders of the Vestibular System
The vestibular system is not necessary for our survival, as studies of people born without this sen- sory system have demonstrated. Often, people whose pregnant mothers had syphilis or German measles are born without vestibular systems. These people are able to stand upright with respect to gravity and can even dive blindfolded into a swimming pool, thanks to the receptors in their muscles and joints. Therefore, disorders of the vestibular system produce annoying, but not life- threatening, symptoms. For example, those individuals with disease of the peripheral vestibular system, such as viral infections that invade the vestibular organs, have difficulty determining visual vertical. They typically are between 58 and 308 off from vertical when asked to indicate vertical on various testing instruments. However, the symptoms of some vestibular disorders can be thoroughly debilitating, as in Meniere’s disease, which produces symptoms of dizziness and unsteadiness (Anderson & Harris, 2001; Di Girolamo, Picciotti, Sergi, D’Ecclesia, & Di Nardo, 2001). Some individuals with Meniere’s disease are helped by surgical removal of the vestibular system (Neely, 2001).
The vestibular system relies on movement of fluid in the semicircular canals and in the utricle and saccule to produce stimulation of the hair cells. Due to the physical property of inertia (resistance to movement), the fluid in these vestibular organs moves slowly. And, when a change in direction occurs, the fluid in the semicircular canals changes direction after a considerable time lag. For this reason, the information reaching the brain from the vestibular system is largely inaccurate. Many of the disorders involving the vestibular system are due to the inaccuracies of this sensory system.
For example, dizziness, or vertigo, occurs when there is a conflict between the information coming from the vestibular system and that coming from the visual system (Herdman, 2010). For example, when an individual spins around in circles, the fluid in that person’s semicircular canals moves in the opposite direction. However, when that individual stops suddenly, the fluid continues in the original direction and then abruptly changes direction, which is similar to what would happen to a person riding in a car that makes a sudden stop. Think about what happens when you slam on the brakes of your car. At first, your body lurches forward because you are heading in a forward direction, and then your body is flung backward. Your vestibular system reacts in the same way. When you stop spinning, the fluid in the semicircular canals pushes your hair cells in the opposite direction to which they were originally pulled, and the message is sent to the brain that the body is now moving in the opposite direction. The eyes, however, tell the brain that the body has stopped moving, and postrotational vertigo results (post means “after” in Latin).
Adaptation of the vestibular system can lead to problems, too. Have you ever been on a cruise that lasted for several days? I haven’t, but once I took a train from Chicago to San Francisco, a trip that lasted 3 days, with the same effect. At first, while on a cruise (or on a train), you are very aware of the movement of the vessel and might even feel seasick, due to prolonged stimulation of the vestibular system. But after a day or so, you are no longer aware of the movement because of adaptation of the vestibular system. However, when you get off the boat or train, the earth under your feet feels as if it is moving and rolling. This hallucination occurs because your vestibular sys- tem, which had adapted to the movement of the boat (or train), suddenly begins firing again, and the brain misinterprets this sudden activation of the vestibular system as movement.
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CHAPTER 7Section 7.6 Chapter Summary
People who spin for a living, like ballerinas and figure skat- ers, have vestibular systems that are permanently adapted. We can demonstrate this by having the ballerina or skater spin in circles and then observe his or her eyes. A normal person who spins in circles will show nystagmus, or oscilla- tion of the eyeballs, as you learned earlier in this section. However, a professional dancer or skater will not show any evidence of nystagmus, which is a sign that the vestibular system is not responding to the spinning movement.
As people age, their vestibular systems deteriorate, produc- ing problems such as dizziness and faulty vestibular reflexes in many elderly individuals (Matheson, Darlington, & Smith, 1999). For most people, a great deal of compensation takes place within the central nervous system, so that they do not show signs of vestibular deterioration. However, for those aged individuals with extremely impaired vestibular sys- tems, the resulting dizziness has profound effects, produc- ing anxiety and loss of confidence, and it may lead to falls. This dizziness is a serious problem for the elderly, especially someone who wishes to live independently.
7.6 Chapter Summary The Somatosensory System
• Somatosensory receptors are located in the skin, muscles, joints, and tendons and typi- cally respond to mechanical stimuli.
• Somatosensation includes skin sensations, kinesthesia, proprioception, and interoception. • Kinesthesia is the ability to sense movement of the body, whereas interoception is the
sensation that arises from internal organs. The skin can sense pressure, temperature, pain, and vibration.
• Pacinian corpuscles respond to pressure, free nerve endings respond to pain, Ruffini’s endings respond to warm sensations, Krause’s end-bulbs respond to cold, and stretch receptors respond to stretch in muscles, tendons, and joints.
• The lemniscal system relays information about pressure and stretch by way of large diam- eter, myelinated A-fibers. The extralemniscal system relays information about tempera- ture and pain by way of thin, unmyelinated C-fibers.
• The primary somatosensory cortex is located in the postcentral gyrus in the parietal lobe.
Somatosensory Processing • Information for somatosensory processing is relayed to the primary somatosensory cortex
in the parietal lobe. • Somatosensory information may also be processed along “What” and “Where” streams in
the secondary somatosensory cortex.
Comstock/Thinkstock
Photo 7.5 Ballerinas have vestibu- lar systems that are permanently adapted.
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CHAPTER 7Section 7.6 Chapter Summary
• The somatosensory “What” system involves the inferior parietal cortex. Damage to this area results in tactile agnosia, a disorder in which a person cannot identify objects by their touch.
• The somatosensory “Where” system involves the posterior parietal lobe, an area also involved in processing visual “Where” information.
• The Gate-Control Theory of Pain has been proposed to explain how we respond to and control the response to painful stimuli.
• Most treatments for pain appear to activate the endorphin pain-inhibitory systems or both. Treatments for pain include drugs, counterirritation, acupuncture, and transcutane- ous electrical nerve stimulation (TENS).
The Olfactory System • Substances that have an odor are called odorants. • Olfactory receptors are located at the top of the nasal cavity and are chemoreceptors
stimulated by chemicals carried in the air. • The olfactory nerve (cranial nerve I) relays information about odorants from the recep-
tors to the olfactory lobe, which contains special structures, called glomeruli, that process information about only one type of odor.
• Information about smell is sent to two different areas in the cerebral cortex, the olfac- tory cortex in the temporal lobe and the prefrontal cortex. The primary olfactory cortex is located in the temporal lobe. The secondary olfactory cortex is in the orbito-frontal prefrontal cortex, located directly behind the eyeball sockets.
• Women consistently perform better than men in tests of odor detection and identification. • An accessory olfactory system transmits information about pheromones to the brain. Sen-
sory receptors for the accessory olfactory system are located in the vomeronasal organ in the floor of the nasal cavity.
• Anosmia is the inability to smell and can be caused by infections, genetic abnormalities, head trauma, brain disorders, and tumors.
The Taste System • Taste receptors are chemoreceptors, which respond to five primary tastes: sweet, sour,
salty, bitter, and umami. • Taste receptors respond to chemicals dissolved in water. • The taste receptors are found in the linings of the mouth and throat, especially in struc-
tures called taste buds that are located on papillae on the tongue. • Information about taste is sent from the taste receptors via cranial nerves to the
nucleus of the solitary tract and on to the thalamus and the primary taste cortex in the frontal lobe.
• Ageusia is the inability to taste, whereas dysgeusia is a disagreeable taste in the mouth produced by an infection, medication, brain tumor, or chemotherapy.
• Unlike the other perceptual systems discussed in this chapter, the olfactory and taste sys- tems do not appear to separate into functional “What” and “Where” streams.
The Vestibular System • The vestibular system, like the somatosensory system, has mechanoreceptors, which are
located in the utricles, saccules, and semicircular canals. These receptors, called hair cells, are sensitive to head movements and head position with respect to gravity.
• Information from the vestibular receptors is transmitted to the brain by way of the ves- tibular branch of the auditory nerve (cranial nerve VIII).
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CHAPTER 7Key Terms
A-fibers Myelinated axons with a large diam- eter; they relay information about pressure and stretching to the brain.
accessory olfactory system The system that transmits information about pheromones, the chemical signals that regulate sexual and social behaviors.
• A number of different pathways carry information from the hair cells in the vestibular sys- tem to various structures in the central nervous system, including the cerebellum, motor neurons that control eye movements, the spinal cord, and the vagus nerve.
• Nystagmus is the oscillation of the eyes following continuous stimulation of the vestibular system.
• Disorders associated with the vestibular system include motion sickness, Meniere’s dis- ease, and vertigo.
• Motion sickness occurs when stimulation of the vestibular system triggers the vagus nerve. Meniere’s disease is a vestibular disorder that produces dizziness and unsteadi- ness. Dizziness, also called vertigo, occurs when the brain receives conflicting information from the vestibular and visual systems.
Questions for Thought
1. Why are some forms of pain control more effective than other forms? 2. Why do women generally have a better sense of smell than men? 3. Is the vestibular system really necessary? Back up your answer. 4. What kinds of information are processed in the primary somatosensory cortex? What
about the secondary somatosensory cortex? 5. Which brain areas have been implicated in the perception of smell and taste? 6. What is the main purpose of the vestibular system? How does this system accomplish its
main purpose?
Web Links
The Medline Plus website, a service of the U.S. National Library of Medicine and the National Institutes of Health, supplies information on taste and smell disorders. Here you will find exten- sive resources on different disorders and conditions, videos, and references to expand your knowledge of the subject. http://medlineplus.gov/
The Vestibular Disorders Association (VEDA) website provides excellent information on under- standing vestibular disorders. The site is a great foundational resource for learning more about the numerous vestibular disorders, treatment, and strategies for tackling the challenges of living with the disorder. http://vestibular.org/
The Mayo Clinic provides basic information, expert answers, and resources on anosmia. Visit the website to learn more about the loss of smell. http://MayoClinic.com/health-information
Key Terms
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CHAPTER 7Key Terms
ageusia An inability to taste.
allodynia An abnormal pain response to a normally nonpainful stimulus that is observed in individuals who have suffered tissue and nerve damage.
analgesia The absence of pain without loss of consciousness.
anosmia An inability to smell odors.
C-fibers Thin, unmyelinated axons that relay information about pain and temperature to the brain.
dysgeusia A disagreeable taste in the mouth due to infection, medication, tumors, or chemotherapy.
extralemniscal pathway The somatosensory pathway that relays information about pain and temperature to the brain.
Gate-Control Theory of Pain A theory about why people respond in different ways to identically painful stimuli; it states that pain messages can be prevented from reaching the cortex by “closing the gate.”
glomeruli Special structures in the olfactory bulb that each process information about one kind of odor.
inferior parietal cortex The region of the brain that is associated with the “What” system for somatosensation.
interoception The sense that arises from one’s internal organs.
kinesthesia The ability to sense movement.
lemniscal pathway The somatosensory path- way that relays information about pressure and stretching to the brain.
mechanoreceptors Receptors that respond to mechanical stimulation, such as pulling, stretching, or vibrating.
nystagmus Oscillation of the eyes following stimulation of the vestibular system.
oculovestibular reflexes Automatic eye move- ments made to compensate for movements of the head.
odorants Substances that have an odor.
olfaction The sense of smell.
olfactory receptors Neurons that respond to chemicals associated with odors.
phantom limb pain A type of chronic pain associated with the perception of pain in an amputated limb.
pheromones Chemical signals that regulate sexual and social behaviors in some species.
posterior parietal cortex The region of the brain that processes “Where” information from the somatosensory system, as well as “Where” information from the visual system.
postrotational vertigo Dizziness that follows spinning or rotation of the head or body.
potentiation A phenomenon in which one taste stimulus causes a receptor to respond more intensely to another stimulus.
primary somatosensory cortex The most anterior part of the parietal lobe, which pro- cesses sensory information from the skin and muscles.
primary taste cortex An area of the fron- tal lobe just above the temporal lobe that receives information about taste stimuli from the thalamus.
primary tastes The five tastes of the taste system: sweet, sour, salty, bitter, and umami.
proprioception The ability to know where a body part is in space.
saccule A vestibular structure that signals information about the position of the head with respect to gravity.
semicircular canals Vestibular structures that respond to changes in head movement.
somatosensory receptors Receptors in the skin, muscles, joints, and tendons.
somatosensory system The sensory system that relays information about the body to the brain.
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CHAPTER 7Key Terms
Stereochemical Theory of Odor A theory that explains how specific odorants excite olfactory sensory neurons: Each odorant is a chemical substance that has a particular shape, and each shape fits into the receptor site like a key fits into a lock.
stretch receptors Mechanoreceptors that respond to stretching.
substantia gelatinosa An area in the dorsal horn of the spinal cord and medulla where the transmission of pain messages to the cere- brum can be inhibited.
tactile agnosia A somatosensory disorder in which the affected individual cannot recog- nize objects through touch; it is associated with damage to the inferior parietal cortex.
taste buds Tiny structures on the tongue that contain taste receptors.
taste receptors Specialized cells that respond to chemicals dissolved in water.
umami The taste receptor that responds to glutamate and has its own specific receptors on the tongue and a special processing area in the cerebral cortex.
utricle A vestibular structure that signals information about the position of the head with respect to gravity.
vertigo Dizziness.
vestibular system The sensory system that responds to changes in head movement and to gravity.
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