The : 353 given bud, tight junctions link the apical ends of adjacent cells G protein-coupled receptors. In the current model for salty together, limiting movement of molecules between the cells. tastes, Na + enters the presynaptic cell through an apical The apical membrane of a taste cell is modified into microvilli channel and depolarizes the taste cell, resulting in exocytosis to increase the amount of surface area in contact with the en­ of the neurotransmitter serotonin. Serotonin in turn excites vironment (Fig. 10-16c). the primary gustatory neuron. For a substance (tastant) to be tasted, it must first dissolve Transduction mechanisms for sour tastes are more contro­ in the saliva and mucus of the mouth. Dissolved taste ligands versial, complicated by the fact that increasing H+, the sour then interact with an apical membrane protein (receptor or taste signal, also changes pH. There is evidence that H+ acts on channel) on a taste cell (Fig. 10-16c). Although the details of ion channels from both extracellular and intracellular sides of signal transduction for the five taste sensations are still contro­ the membrane, and the transduction mechanisms remain un­ versial, interaction of a taste ligand with a membrane protein certain. Ultimately, H+-mediated depolarization of the presyn­ initiates a signal transduction cascade that ends with a series of aptic cell results in serotonin release, as described for salt taste action potentials in the primary sensory neuron. above. The mechanisms of taste transduction are a good example Neurotransmitters (ATP and serotonin) from taste cells ac­ of how our models of physiological function must periodically tivate primary gustatory neurons whose axons run through cra­ be revised as new research data are published. For many years nial nerves VII, IX, and X to the medulla, where they synapse. the widely held view of taste transduction was that an individ­ Sensory information then passes through the thalamus to the ual taste cell could sense more than one taste, with cells differ­ gustatory cortex (see Fig. 10-4). Central processing of sensory ing in their sensitivities. However, gustation research using mo­ information compares the input from multiple taste cells and lecular biology techniques and knockout mice [ ~ jJ 292J interprets the taste sensation based on which populations of currently indicates that each taste cell is sensitive to only one neurons are responding most strongly. Signals from the sensory 10 taste. neurons also initiate behavioral responses, such as feeding, and In the old model, all taste cells formed synapses with pri­ feedforward responses [ ~ fl. 2ll-l-J that activate the digestive mary sensory neurons called gustatory neurons. Now it has system. been shown that there are two different types of taste cells, An interesting psychological aspect of taste is the phe­ and that only the taste cells for salty and sour tastes (type III nomenon named specific hunger. Humans and other animals or presynaptic cells) synapse with gustatory neurons. The that are lacking a particular nutrient may develop a craving for presynaptic taste cells release the neurotransmitter serotonin that substance. Salt appetite, representing a lack of Na+ in the byexocytosis. body, has been recognized for years. Hunters have used their The taste cells for sweet, bitter, and umami sensations knowledge of this specific hunger to stake out salt licks because (type II or receptor cells) do not form traditional synapses. they know that animals will seek them out. Salt appetite is di­ Instead they release ATP through gap junction-like channels, rectly related to Na+ concentration in the body and cannot be and the ATP acts both on sensory neurons and on neighboring assuaged by ingestion of other cations, such as Ca2 + or K+. presynaptic cells. This communication between neighboring Other appetites, such as cravings for chocolate, are more diffi­ taste cells creates complex interactions. cult to relate to specific nutrient needs and probably reflect complex mixtures of physical, psychological, environmental, Taste Transduction Uses Receptors and cultural influences. and Channels The details of taste cell signal transduction, once thought to be CONCEPT CHECK relatively straightforward, are also more complex than scien­ 14. With what essential nutrient is the umami taste sensation as­ tists initially thought (Fig. 10-17 e ). The type II taste cells for sociated? bitter, sweet, and umami tastes express different G protein­ 1S. Map or diagram the neural pathway from a presynaptic taste coupled receptors, including about 30 variants of bitter recep­ cell to the gustatory cortex. Answers p. 383 tors. In type II taste cells, the receptor proteins are associated with a special G protein called gustducin. Gustducin appears to activate multiple signal transduc­ THE EAR: HEARING tion pathways. Some pathways release Ca2 + from intracellular The ear is a sense organ that is specialized for two distinct func­ stores, while others open cation channels and allow Ca 2 + to tions: hearing and equilibrium. It can be divided into external, enter the cell. Calcium signals then initiate ATP release from middle, and inner sections, with the neurological elements the type II taste cells. housed in and protected by structures in the . The In contrast, salty and sour transduction mechanisms vestibular complex of the inner ear is the primary sensor for both appear to be mediated by ion channels rather than by equilibrium. The remainder of the ear is used for hearing. 354 Chapter 10 Sensory Physiology

0- Sweet, umami, Sour or bitter li gand @ Gustducin 0 1 GPCR /0 Ligands activate the taste cell.

Various intracellular pathways are activated.

~) Ca2• signal in the cytoplasm triggers exocytosis or ATP formation .

• Serotonin o : - Neurotransmitter or ATP is released.

""":-­--­ Primary gustatory --~,. , neurons «) Primary sensory neuron fires and action potentials are sent to the brain. e FIGURE 10-17 Summary of taste transduction. Each taste cell senses only one type of ligand. Receptor cells with G protein-coupled membrane receptors bind either bitter, sweet, or umami ligands and release ATP as a signal molecule. Sodium ion for salt taste enters presynaptic cel ls through ion channels and triggers exocytosis of serotonin. It is unclear whether H+ for sour taste acts intracellularly or extracellularly.

The external ear consists of the , or pinna, and the ing. Colds or other infections that cause swelling can block the (Fig. 10-18 e ). The pinna is another exampJe of an and result in fluid buildup in the . If important accessory structure to a sensory system, and it varies bacteria are trapped in the middle ear fluid, the ear infection in shape and location from species to species, depending on known as otitis m edia [oto-, ear + -itis, inflammation + media, the animals' survival needs. The ear canal is sealed at its inter­ middle] results. nal end by a thin membranous sheet of tissue called the Three small bones of the middle ear conduct sound from tympanic membrane, or . the external environment to the inner ear: the [ham­ The tympanic membrane separates the external ear from mer], the [anvil], and the [stirrup]. The three the middle ear, an air-filled cavity that connects with the phar­ bones are connected to one another with the biological equiv­ ynx through the eustachian tube. The eustachian tube is nor­ alent of hinges. One end of the malleus is attached to the tym­ mally collapsed, sealing off the middle ear, but it opens tran­ panic membrane, and the stirrup end of the stapes is attached siently to allow middle ear pressure to eqUilibrate with to a thin membrane that separates the middle ear from the atmospheric pressure during chewing, swallOwing, and yawn­ inner ear. The Ear: Hearing 355

waves, but there is no noise unless someone or something is EME RGING CONCEPTS present to process and perceive the wave energy as sound. Sound is the brain's interpretation of the frequency, ampli­ tude, and duration of sound waves that reach our . Our CHANGING TASTE brains translate frequency of sound waves (the number of Sweet receptors respond to sugars, and umami wave peaks that pass a given point each second) into the pitch receptors respond to glutamate, covering two of the of a sound. Low-frequency waves are perceived as low-pitched three major groups of nutritious biomolecules. But sounds, such as the rumble of distant thunder. High-frequency what about fats? For years physiologists thought it waves create high-pitched sounds, such as the screech of finger­ was fat's texture that made it appealing, but now it appears that the tongue may have receptors for nails on a bl ackboard. long-chain fatty acids, such as oleic acid [ ~r lfl ). Sound wave frequency (Fig. 10-19b) is measured in waves Research in rodents has identified a membr·ane re­ per second, or hertz (Hz). The average human ear can hear ceptor called CD36 that lines taste pores and binds sounds over the frequency range of 20-20,000 Hz, with the fats. Activation of the receptor helps trigger the most acute hearing between 1000-3000 Hz. Our hearing is not feedforward digestive reflexes that prepare the as acute as that of many other animals, just as our sense of digestive system for a meal. Cur-rently evidence is smell is less acute. Bats listen for ultra-high-frequency sound lacking for a similar receptor in humans, but "fatty" waves (in the kilohertz range) that bounce off objects in the may turn out to be a sixth taste sensation. dark. Elephants and some birds can hear sounds in the infra­ And what would you say to the idea of taste sound (very low frequency) range. buds in your gut? Scientists have known for years Loudness is our interpretation of sound intensity and is that the stomach and intestines have the ability to influenced by the sensitivity of an individual's ear. The inten­ sense the composition of a meal and secrete appro­ o priate hormones and enzymes. Now it appears that sity of a sound wave is a function of the wave amplitude gut chemoreception is being mediated by the same (Fig . 1O-19b). Intensity is measured on a logarithmic scale in receptors and signal transduction mechanisms that units called decibels (dB). Each 10-dB increase represents a lO-fold occur in taste buds on the tongue. Studies have increase in intensity. found the T1 R receptor proteins for sweet and Normal conversation has a typical noise level of about 60 dB. umami tastes as well as the G protein gustducin in Sounds of 80 dB or more can damage the sensitive hearing re­ various cells in rodent and human intestines. ceptors of the ear, resulting in hearing loss. A typical heavy metal rock concert has noise levels around 120 dB, an intensity that puts listeners in immediate danger of damage to their hearing. The amount of damage depends on the duration and frequency of the noise as well as its intensity. The inner ear consists of two major sensory structures. The vestibular apparatus with its is the sensory CONCEPT CHECK transducer for our sense of equilibrium, described in the follow­ 16. What is a kilohertz? Answers p. 383 ing section. The of the inner ear contains sensory re­ ceptors for hearing. On external view the cochlea is a m embra­ Sound Transduction Is a Multistep Process nous tube that lies coiled like a snail shell within a bony cavity. Two membranous disks, the (to which the stapes Hearing is a complex sense that involves multiple transductions. is attached) and the , separate the liquid-filled Energy from sound waves in the air becomes CD mechanical cochlea from the air-filled middle ear. Branches of cranial nerve vibrations, then ® fluid waves in the cochlea. The fluid waves VIII, the vestibulococl1lear nerve, lead from the inner ear to the open ion channels in l1air cells, the sensory receptors for hearing. brain. Ion flow into hair cells creates @ electrical signals that release (3) neurotransmitter (chemical signal), which in turn triggers ® ac­ Hearing Is Our Perception of Sound tion potentials in the primary auditory neurons. These transduction steps are shown in Figure 10-20 • . Hearing is our perception of the energy carried by sound WaI'es, Sound waves striking the outer ear are directed down the ear which are pressure waves with alternating peaks of compressed canal until they hit the tympaniC membrane and cause it to vi­ air and valleys in which the air molecules are farther apart brate (first transduction). The tympaniC membrane vibrations (Fig. 10-19a e ). The classic question about hearing is, "If a tree are transferred to the malleus, the incus, and the stapes, in that falls in the forest with no one to hear, does it make a noise?" order. The arrangement of the three connected middle ear The physiological answer is no. The falling tree emits sound 356 Chapter 10 Sensory Physiology

THE EAR

EXTERNAL EAR MIDDLE EAR \ INNER EAR

~------~~~ \,\~--~------~~! \ , The oval window and the round window separate The pinna \ \ the fluid-filled inner ear from the air-filled middle ear. directs sound \ \ waves into \ \ the ear \ Malleus \ Semicircular Oval \ \ canals window Nerves \ \ Stapes '. \

Tympanic membrane

Eustachian vein tube

• FIGURE 10-18 bones creates a "lever" that multiplies the force of the vibration Movement of the opens or closes ion chan­ (amplification ) so that very little sound energy is lost due to fric­ nels on membranes, creating electrical signals (third tion. If noise levels are so high that there is danger of damage transduction). These electrical signals alter neurotransmitter re­ to the inner ear, small muscles in the middle ear can pull on lease (fourth transduction). Neurotransmitter binding to the the bones to decrease their movement and thereby dampen primary auditory neurons initiates action potentials (fifth sound transmission to some degree. transduction) that send coded information about sound As the stapes vibrates, it pulls and pushes on the thin tis­ through the cochlear branch of the vestibulocochlear nerve (cranial sue of the oval window, to which it is attached. Vibrations at nerve VlII) and the brain. the oval window create waves in the fluid-filled channels of the cochlea (second transduction). As waves move through the The Cochlea Is Filled with Fluid cochlea, they push on the fle xible membranes of the cochlear The transduction of wave energy into action potentials takes duct and bend sensory hair cells inside the duct. The wave en­ place in the cochlea of the inner ear. Uncoiled, the cochlea can ergy dissipates back into the air of the middle ear at the round be seen to be composed of three parallel, fluid-filled channels: window. The Ear: Hearing 357

RUNNING PROBLEM

Anant reports to the otolaryngologist that he never knows when his attacks of dizziness will strike and that they last from 10 min­ utes to an hour. They often cause him to vomit. He also reports that he has a persistent low buzzing sound in one ear and that he does not seem to hear low tones as well as he could before the attacks started. The buzzing sound (tinnitus) often gets worse during his dizzy attacks. Tuning fork Question 2: (a) Sound waves alternate peaks of compressed air and valleys where Subjective tinnitus occurs when an abnormality somewhere the air is less compressed. along the anatomical pathway for hearing causes the brain to perceive a sound that does not exist outside the auditory sys­ tem. Starting from the ear canal, name the auditory struc­ (1) tures in which problems may arise. / 1 Wavelength 1----41 339 e

Intensity -jAmPlitude (dB) (dB) at the tip of the cochlea through a small opening known as the helicotrema [, a spiral + tJ'ema, hole]. The cochlear duct is o o a dead-end tube but it connects to the vestibular apparatus Time (sec) 0.25 through a small opening. The fluid in the vestibular and tympaniC ducts is similar in (2) ion composition to plasma and is known as . The cochlear duct is filled with secreted by epithelial cells in the duct. Endolymph is unusual because it is more like intracellular fluid than extracellular fluid in composition, with I",e"(~i~ ~nVnVVn nVnVnVV n ffvfiv fi1 r~~rli,"de high concentrations of K+ and low concentrations of Na +. The cochlear duct contains the , composed of hair cell receptors and support cells. The organ of Corti sits 0.25 on the and is partially covered by the o Time (sec) • [tectorium, a cover], both flexible tissues (b) Sound waves are distinguished by their amplitude, measured in that move in response to fluid waves passing through the decibels (dB), and frequency, measured in hertz (Hz). vestibular duct (Fig. 10-21). As the waves travel through the cochlea, they displace basilar and tectorial membranes, creat­ FIGURE QUESTIONS ing up-and-down oscillations that bend the hair cells. Hair cells, like taste cells, are non-neural receptor cells . • What are the frequencies of the sound waves in graphs (1) and (2) The apical surface of each hair cell is modified into 50-100 stiff­ in Hz (waves/second)? ened cilia known as , arranged in ascending height • Which set of sound waves would be interpreted as having lower pitch? (Fig. 10-22a e ). The longest cilium of each hair cell, called a [kinein, to move] is embedded in the overlying tec­ • FIGURE 10-19 Sound waves torial membrane. If the tectorial membrane moves, the embed­ ded kinocilia do also. This movement is transmitted to the stereocilia of the hair cell. (1) the vestibular duct, or scala vestibuli [scala, stairway; When hair cells move in response to sound waves, their vestibulum, entrance]; (2) the central cochlear duct, or scala stereocilia flex, first one way, then the other. The stereocilia are media [media, middle]; and (3) the tympanic duct, or scala tym­ attached to each other by protein bridges called tip links . The pani [tympal1ol1 , drum] (Fig. 10-21 e ). The vestibular and tym­ tip links act like little springs and are connected to gates that panic ducts are continuous with each other, and they connect 358 Chapter 10 Sensory Physiology

Sound waves strike e The sound wave e The stapes is attached to the tympanic energy is transferred the membrane of the oval membrane and to the three bones window. Vibrations of the become vibrations. of the middle ear, oval window create fluid which vibrate. waves within the cochlea.

---'r l--t:+­-­ Vestibular duct (perilymph)

0+---+---- Cochlear duct (endolymph)

-,f-.,.,...--- Tympanic duct (perilymph)

Tympanic Round membrane window

The fluid waves push on the e Neurotransmitter release Cit Energy from the waves flexible membranes of the onto sensory neurons transfers across the cochlear duct. Hair cells bend creates action potentials cochlear duct into the and ion channels open, that travel through the tympanic duct and is creating an electrical signal that to dissipated back into alters neurotransmitter release. the brain. the middle ear at the round window.

• FIGURE 10-20 Sound transmission through the ear open and close ion channels in the cilia membrane. When the neurons must be able to respond to sounds of nearly 20,000 hair cells and cilia are in a neutral position, about 10% of the waves per second, the highest frequency audible by a human ear. ion channels are open, and there is a low level of tonic neuro­ transmitter released onto the primary sensory neuron. CONCEPT CHECK When waves deflect the tectorial membrane so that cilia 17. Normally when cation channels on a cell open, either Na + or bend toward the tallest members of a bundle, the tip links pop 2 2 Ca + enters the cell. Why is it K+ rather than Na+ that enters more channels open, so cations (primarily K+ and Ca +) enter hair cells when cation channels openl Answef5: p. 383 the cell, which then depolarizes (Fig. 1O-22b). Voltage-gated 2 Ca + channels open, neurotransmitter release increases, and Sounds Are Processed First in the Cochlea the sensory neuron increases its firing rate. When the tectorial The processes sound waves so that they can be membrane pushes the cilia away from the tallest members, the discriminated by location, pitch, and loudness. Localization of springy tip links relax and all the ion channels close. Cation in­ sound is a complex process that requires sensory input from flux slows, the membrane hyperpolarizes, less transmitter is re­ both ears coupled with sophisticated computation by the brain leased, and sensory neuron firing decreases (Fig. lO-22c). (see Fig. lO-S). In contrast, the initial processing for pitch and The vibration pattern of waves reaching the inner ear is loudness takes place in the cochlea of each ear. thus converted into a pattern of action potentials going to the Coding sound for pitch is primarily a function of the basi· CNS. Because tectorial membrane vibrations reflect the fre­ lar membrane. This membrane is stiff and narrow near its quency of the incoming sound wave, the hair cells and sensory THE COCHLEA Oval Vestibular Cochlear Organ of duct duct Corti

Uncoiled

\ \ \ , Round Tympanic Basilar I window duct membrane I I

, ~\r\

Vestibular duct ,r r " t.'

Cochlear duct / ",' (~ :

Tectorial membrane /- ~ r ( I A .....~"-

Organ of Corti 1, 1 ~~ ..,--. - .. (\1, 1 ~'""~

The movement of the tectorial membrane moves the cilia on transmits action the hair cells. potentials from Basilar the hair cells to membrane the auditory / / cortex, / /

Cochlear duct

Tympanic { ' .!.l....[- [ :::: Nerve fibers of duct ~- : - I .. I cochlear nerve

• FIGURE 10-21

359 360 Chapter 10 Sensory Physiology

(a) At rest: About 10% of the ion (b) Excitation: When the hair cells bend in (c) Inhibition: If the hair cells bend in the channels are open and a tonic signal one direction, the cell depolarizes, which opposite direction, ion channels close, is sent by the sensory neuron. increases action potential frequency in the cell hyperpolarizes, and sensory the associated sensory neuron. neuron signaling decreases.

Tip link \ oh,oo,', Stereocilium Ul Som, ~~o" Channels closed. r U'Ichannels 1¥6~t) open. Less cation entry ~ 1open Cation entry hyperpolarizes cell. Hair cell I depolarizes cell.

Primary sensory neuron

Action potentials Action potentials increase No action potentials

/::" £ Action potentials in primary sensory neuron Time

0

mV

-30

Release Release

Membrane potential Excitation opens Inhibition closes of hair cell ion channels ion channels

e FIGURE 10-22 Signal transduction in hair cells. The stereocilia of hair cells have "trap doors" that close off ion channels. These openings are controlled by protein-bridge tiplinks connecting adjacent cilia.

attachment between the round and oval windows but widens sponse to frequency transforms the temporal aspect of fre­ and becomes more flexible near its distal end (Fig. lO-23a e ). quency (number of sound waves per second) into spatial coding High-frequency waves entering the vestibular duct create for pitch by location along the basilar membrane (Fig. lO-23b). maximum displacement of the basilar membrane close to the A good analogy is a piano keyboard, where the location of a key oval window and consequently are not transmitted very far tells you its pitch. The spatial coding of the basilar membrane along the cochlea. Low-frequency waves travel along the is preserved in the auditory cortex as neurons project from hair length of the basilar membrane and create their maximum dis­ cells to corresponding regions in the brain. placement near the flexible distal end. This differential re­ The Ear: Hearing 361

Low frequency tion that is processed into the timing of sound, and others High frequency (low pitch) (high pitch) carry information that is processed into the sound quality. Basilar membrane ...... From the medulla, secondary sensory neurons project to Stiff region near Flexible region two nuclei in the pons, one ipsilateral (on the same side of the round window near helicotrema body) and one contralateral (on the opposite side). Splitting (distal end) sound signals between two ascending tracts means that each (a) The basilar membrane has variable sensitivity to sound wave frequency along its length. side of the brain gets information from both ears. Ascending tracts from the pons then synapse in nuclei in the midbrain and thalamus before projecting to the auditory cortex (see Fig. 10-4). Basilar Helicotrema Collateral pathways take information to the reticular formation membrane and the cerebellum. The localization of a sound source is an integrative task that requires simultaneous input from both ears. Unless sound Stapes is coming from directly in front of a person, it will not reach both ears at the same time (see Fig. 10-5). The brain records the time differential for sound arriving at the ears and uses com­ plex computation to create a three·dimensional representation i3 i ~1 of the sound source. 0 10 20 ~ j 30 Hearing loss May Result from Mechanical ~ O~____:::::-_ or Neural Damage r10 There are three forms of hearing loss: conductive, central, and sensorineural. In conductive hearing loss, sound cannot be trans­ 13: ~ mitted through either the external ear or the middle ear. The -o 0 j0 10 causes of conductive hearing Joss range from an ear canal (5 20 30 E plugged with earwax (cerumen), to fluid in the middle ear from an infection, to diseases or trauma that impede vibration of the malleus, incus, or stapes. Correction of conductive hearing loss includes microsurgical techniques in which the bones of the j :J~ I I middle ear can be reconstructed. o 10 20 30 Central hearing loss results either from damage to the - Distance from oval window (mm)­ neural pathways between the ear and cerebral cortex or from (b) The frequency of sound waves determines the displacement damage to the cortex itself, as might occur from a stroke. This of the basilar membrane. The location of active hair celis creates form of hearing loss is relatively uncommon. a code that the brain translates as information about the pitch of sound. Sensorineural hearing loss arises from damage to the struc­ tures of the inner ear, including death of hair cells as a result of • FIGURE 10-23 Sensory coding for pitch takes place loud noises. The loss of hair cells in mammals is currently irre­ along the basilar membrane. Graph adapted from G. Von versible. Birds and lower vertebrates, however, are able to re­ Bekesy, Experiments in Hearing (McGraw-Hili: New York, 1960). generate hair cells to replace those that die. This discovery has researchers exploring strategies to duplicate the process in Loudness is coded by the ear in the same way that signal mammals, including transplantation of neural stem cells and strength is coded in somatic receptors. The louder the noise, gene therapy to induce nonsensory cells to differentiate into the more rapidly action potentials fire in the sensory neuron. hair cells. A therapy that replaces hair cells would be an important Auditory Pathways Project advance because the incidence of hearing loss in younger peo­ to the Auditory Cortex ple is increasing because of prolonged exposure to rock music Once the cochlea transforms sound waves into electrical sig­ and environmental noises. Ninety percent of hearing loss in nals, sensory neurons transfer this information to the brain. the elderly-called presbycusis [presbys, old man + akoustikos, The cochlear (auditory) nerve is a branch of cranial nerve VIII, able to be heard]-is sensorineural. Currently the primary treat­ ment for sensorineural hearing loss is the use of hearing aids, the vestibulocochlear nerve [ ~ p . 310]. Primary auditory neu­ rons project from the cochlea to cochlear nuclei in the medulla but amazing results have been obtained with cochlear implants oblongata (Fig. 10-24 e ). Some of these neurons carry informa- attached to tiny computers (see Biotechnology box). 362 Chapter 10 Sensory Physiology

• FIGURE 10-24 Auditory pathways

Right auditory cortex Left auditory cortex

Cochlear branch of right Cochlear branch of left vestibulocochlear nerve (VIII) vestibulocochlear nerve (VIII)

Hearing is probably our most important social sense. CONCEPT CHECK Suicide rates are higher among deaf people than among those who have lost their sight. More than any other sense, hearing 18. Map or diagram the pathways followed by a sound wave en­ connects us to other people and to the world around us. tering the ear, starting in the air at the outer ear and ending on the auditory cortex. 19 . Why is somatosensory information projected to only one hemisphere of the brain but auditory information is projected to both hemispheres? (Hint: See Fig s. 10-5 and 10-9.) BIOTECHNOLOGY 20. Would a cochlear implant help a person who suffers from nerve deafness? From conductive hearing loss? "- . ." p.383 COCHLEAR IMPLANTS One technique used to treat sensorineural hearing loss is the cochlear implant. The newest cochlear THE EAR: EQUILIBRIUM implants have multiple components. Externally, a micro­ Equilibrium is a state of balance, whether the word is used to phone, tiny computerized speech processor, and trans­ describe ion concentrations in body fluids or the position of the mitter fit behind the ear like a conventional hearing body in space. The special sense of equilibrium has two compo­ aid. The speech processor is a transducer that converts nents: a dynamic component that tells us about our movement sound into electrical impulses. The transmitter con­ through space, and a static component that tells us if our head verts the processor's electrical impulses into radio is not in its normal upright position. Sensory information from waves and sends these signals to a receiver and 8-24 the inner ear and from joint and muscle proprioceptors tells our electrodes, which are surgically placed under the skin. brain the location of different body parts in relation to one an­ The electrodes take electrical signa'is directly into the other and to the environment, Visual information also plays an cochlea and stimulate the sensory nerves. After sur­ important role in equilibrium, as you know if you have ever gery, recipients go through therapy so that they can 0 learn to understand the sounds they hear. Cochlear gone to one of the 360 movie theaters where the scene tilts sud­ implants have been remarkably successful for many denly to one side and the audience tilts with it! profoundly deaf people, allowing them to hear loud Our sense of equilibrium is mediated by hair cells lining noises and modulate their own voices. In the most the fluid-filled vestibular apparatus of the inner ear. These non­ successful cases, individuals can even use the tele­ neural receptors respond to changes in rotational, vertical, and phone. To learn more about cochlear implants, visit horizontal acceleration and pOSitioning. The hair cells function the web site of the National Institute for Deafness just like those of the cochlea, but gravity and acceleration and Other Communication Disorders (www.nidcd.nih. rather than sOLlnd waves provide the force that moves the govlhealthlhearing). stereocilia.