Physiology of hearing. Vestibular analyzer.

Somatic sensory analyzer

 

Physiology of hearing

The organs of hearing and balance are divided into three parts: external, middle, and inner ears. The external and middle ears are involved in hearing only, whereas the inner ear functions in both hearing and balance. The external ear includes the auricle and the external auditory meatus. The external ear terminates medially at the eardrum, or tympanic membrane. The middle ear is an air-.lled space within the petrous portion of the temporal bone, which contains the auditory ossicles. The inner ear contains the sensory organs for hearing and balance. It consists of interconnecting .uid-.lled tunnels and chambers within the petrous portion of the temporal bone.

Auditory Structures and Their Functions

External Ear

ear, external The ear of a mammal is divided into three regions: the external or outer ear, the middle ear, and the inner ear. The external ear is the only part that is visible from the outside and is what people are usually referring to when they talk about their ears. It consists of a skin-covered flap known as the pinna or auricle, which leads like a funnel into the ear canal (external auditory meatus). Apart from the soft earlobe, the pinna possesses a framework of cartilage moulded to form several ridges and depressions, the most important being a cavity known as the concha, which lies just behind the opening to the ear canal.

 

The ear canal, which is also lined by skin, is a tubular structure, about 25 mm long, with a cartilaginous outer region and a bony inner region. Fine hairs and glands (which secrete wax) are found in the outer part. The ear canal terminates at the eardrum (tympanic membrane), which forms the boundary between the external ear and the middle ear. The external ear is responsible for collecting airborne sounds and for protecting the delicate eardrum from mechanical damage.

 

Although experiments carried out in the late nineteenth century provided insights into the role of the external ear in hearing, many textbooks give scant attention to it and even state, quite erroneously, that it is a vestigial structure in human beings, having little function compared with the larger, more erect, and often moveable ears of other mammals. This is largely due to the fact that research on hearing in the twentieth century mainly involved the delivery of sound by headphones, which cover and therefore remove the influence of the pinnae. However, beginning 30 years ago, acoustical measurements using tiny microphones inserted into the ear canals of either real or artificial pinnae have shown how incoming sound waves are modified by the different components of the external ear in ways that aid our ability to detect and localize sounds in the environment.

 

The external ear has two key functions. Firstly, the resonances of the external ear, particularly of the concha and ear canal, increase the sound pressure at the eardrum for some frequencies of sound by as much as 20 dB. In adult humans, this gain in amplitude is greatest at sound frequencies from 2 to 7 kHz. Consequently, sounds in this frequency range are transmitted by the external ear most efficiently, which, in turn, contributes to an improvement in the listener's hearing sensitivity. (It may be significant that the sound of human speech is largely concentrated in this frequency band.)

Secondly, interaction of sound waves with the external ear provides information that helps in judging the location of sound sources. The primary cues for sound localization result from the fact that we have two ears, one on each side of the head. Sounds that lie to one side of the straight-ahead direction differ in their time of arrival and in the amplitude of the sound at the two ears. These differences can be detected by neurons in the brain, which underlie our ability to determine the direction of a sound source. However, studies in humans and other animals have shown that the external ear, by differentially filtering sounds from different directions in space, provides additional information. Therefore, filling the cavities of the pinna or inserting tubes into the ear canals to bypass the pinnae altogether leads to errors in localization of sounds, particularly in the vertical direction, and to a decreased ability to discriminate sounds in front from those behind. Although two ears are definitely better than one for recognizing the positions of sounds, the filtering of sounds in the external ear can enable us to localize sounds under circumstances where the so-called binaural cues are ambiguous or missing. Such monaural listening conditions occur not only in people who are deaf in one ear, but when a sound on one side is too quiet to reach one of the ears, because of the shadowing effect of the head.

The convolutions of the external ear, particularly the concha, act to increase or decrease the amplitude of different frequency components of a sound as it passes from the free field to the eardrum. These filtering effects are dependent on the location of the sound, giving rise to spectral patterns — characteristic variations in amplitude with frequency — that vary with both the horizontal and vertical angle of the sound source. These spectral cues are most useful when the sound contains energy over a wide range of high frequencies. Eliminating the influence of the pinna by wearing headphones — for example, when listening to music on a personal stereo — gives rise to the impression that the sound is located inside the head. However, if sounds in the free field are first recorded with microphones placed in the ear canal, hence spectrally transformed by the pinna, and then played back over headphones, the listener experiences the vivid illusion of a sound originating from a particular direction outside the head. Generating virtual space sounds in this way not only helps in the scientific study of sound localization: computer-generated virtual environments are also used in training simulators and are found in many amusement arcades.

Because no two ears are exactly the same, we might imagine that each person has to learn to use the spectral cues generated by the particular dimensions of his or her own ears. Thus, listeners usually localize less well when listening to sounds as filtered by another person's external ears.

Some mammals, such as cats and bats, can precisely and independently alter the shape and orientation of their pinnae. Dogs tend to ‘prick up their ears’, i.e. raise their pinnae. Cats readily direct their ears toward the source of environmental sounds, usually in concert with movements of the eyes and head. These movements of the pinna appear to optimize sound reception by placing it at the position where the increase in sound pressure provided by the external ear is maximal, and may also help in sound localization. In bats, pinna movements are additionally thought to play an important role in echolocation.

As well as their auditory function, the external ears can help in the regulation of an animal's body temperature, via control of their extensive blood supply; and they may contribute to the threatening gestures made in encounters with other animals. Middle Ear

Medial to the tympanic membrane is the air-filled cavity of the middle ear. Two covered openings, the round and oval windows, on the medial side of the middle ear separate it from the inner ear. Two openings provide air passages from the middle ear. One passage opens into the mastoid air cells in the mastoid process of the temporal bone. The other passageway, the auditory, or eustachian tube, opens into the pharynx and equalizes air pressure between the outside air and the middle ear cavity. Unequal pressure between the middle ear and the outside environment can distort the eardrum, dampen its vibrations, and make hearing difficult. Distortion of the eardrum, which occurs under these conditions, also stimulates pain fibers associated with it. Because of this distortion, when a person changes altitude, sounds seem muffled, and the eardrum may become painful. These symptoms can be relieved by opening the auditory tube to allow air to pass through the auditory tube to equalize air pressure. Swallowing, yawning, chewing, and holding the nose and mouth shut while gently trying to force air out of the lungs are methods used to open the auditory tube.

The middle ear contains three auditory ossicles: the malleus, incus, and stapes, which transmit vibrations from the tympanic membrane to the oval window. The handle of the malleus is attached to the inner surface of the tympanic membrane, and vibration of the membrane causes the malleus to vibrate as well. The head of the malleus is attached by a very small synovial joint to the incus, which in turn is attached by a small synovial joint to the stapes. The foot plate of the stapes .ts into the oval window and is held in place by a .exible annular ligament.

Role of middle ear in sound perception

1.                 Middle ear occupies tympanic cavity. Tympanic membrane forms lateral wall of tympanic cavity. Handle of malleus attaches to point of maximal concavity of tympanic membrane on its inner surface. Other end of malleus is bound to incus by ligaments. Opposite end of incus articulates with stem of stapes.

2.                 Faceplate of stapes lies against membranous labyrinths in oval window, where sound waves are conducted into cochlear. Auditory ossicles increase pressure exerted by sound waves on fluid of cochlear. Thus provides impedance matching between sound waves in air and sound vibrations in fluid of cochlear.

3.                 Tympanic cavity is filled with air. Besides auditory ossicles tympanic cavity also contains tensor tympani muscle and stapedius muscle. There are two windows in medial wall of tympanic cavity, round window and oval window.

Attenuation reflex and adaptation to sound

1.                 It is a reflex that occurs when loud sounds low frequency sounds are transmitted through ossicular system into central nervous system. It occurs after latent period of 40-80 ms.

2.                 Tensor tympani muscle pulls handle of malleus inwards. Stapedius muscle pulls stapes out of oval window. These two forces  are opposite to each other. It causes entire ossicular system to become highly rigid.

3.                 This mechanism reduces ossicular conduction of loud or low frequency sounds. As a result intensity of sound, which comes into inner ear reduces to 30-40 decibels.

Sound waves strike the tympanic membrane and cause it to vibrate. This vibration causes vibration of the three ossicles of the middle ear, and by this mechanical linkage vibration is transferred to the oval window. More force is required to cause vibration in a liquid like the perilymph of the inner ear than is required in air; thus, the vibrations reaching the perilymph must be ampli.ed as they cross the middle ear. The footplate of the stapes and its annular ligament, which occupy the oval window, are much smaller than the tympanic membrane. Because of this size difference, the mechanical force of vibration is ampli.ed about 20-fold as it passes from the tympanic membrane, through the ossicles, and to the oval window.

Two small skeletal muscles are attached to the ear ossicles and re.exively dampen excessively loud sounds. This sound attenuation re.ex protects the delicate ear structures from damage by loud noises. The tensor tympani muscle is attached to the malleus and is innervated by the trigeminal nerve (V). The stapedius muscle is attached to the stapes and is supplied by the facial nerve (VII). The sound attenuation re.ex responds most effectively to low-frequency sounds and can reduce by a factor of 100 the energy reaching the oval window. The reflex is too slow to prevent damage from a sudden noise, such as a gunshot, and it cannot function effectively for longer than about 10 minutes, in response to prolonged noise.

Attenuation reflex  importance

1.                 Attenuation reflex protects basilar membrane of cochlear from damaging vibrations of loud sounds. It masks also low frequency sounds in loud environment. This phenomenon a person to concentrate on high frequency sounds.

2.                 Attenuation reflex is actual also for decrease person's hearing sensitivity to his own speech. Prolonged hearing of a loud sound also lead to transient loss of sensitivity of central auditory neurons because of inhibitory process. It is called central adaptation to sound.

Inner Ear

The tunnels and chambers inside the temporal bone are called the bony labyrinth. Because the bony labyrinth consists of tunnels within the bone, it cannot easily be removed and examined separately. The bony labyrinth is lined with periosteum, and when the inner ear is shown separately, the periosteum is what is depicted. Inside the bony labyrinth is a similarly shaped but smaller set of membranous tunnels and chambers called the membranous labyrinth. The membranous labyrinth is .lled with a clear .uid called endolymph, and the space between the membranous and bony labyrinth is filled with a fluid called perilymph. Perilymph is very similar to cerebrospinal fluid, but endolymph has a high concentration of potassium and a low concentration of sodium, which is opposite from perilymph and cerebrospinal fluid.

The bony labyrinth is divided into three regions: cochlea, vestibule, and semicircular canals. The vestibule and semicircular canals are involved primarily in balance, and the cochlea is involved in hearing. The membranous labyrinth of the cochlea is divided into three parts: the scala vestibuli, the scala tympani, and the cochlear duct.

 

 

(a) The inner ear. The outer surface (gray) is the periosteum lining the inner surface of the bony labyrinth.

(b) A cross section of the cochlea. The outer layer is the periosteum lining the inner surface of the bony labyrinth. The membranous labyrinth is very small in the cochlea and consists of the vestibular and basilar membranes. The space between the membranous and bony labyrinth consists of two parallel tunnels: the scala vestibuli and scala tympani.

(c) An enlarged section of the cochlear duct (membranous labyrinth).

(d ) A greatly enlarged individual sensory hair cell.

 

The oval window communicates with the vestibule of the inner ear, which in turn communicates with a cochlear chamber, the scala vestibuli. The scala vestibuli extends from the oval window to the helicotrema  at the apex of the cochlea; a second cochlear chamber, the scala tympani, extends from the helicotrema, back from the apex, parallel to the scala vestibuli, to the membrane of the round window.

The scala vestibuli and the scala tympani are the perilymph-filled spaces between the walls of the bony and membranous labyrinths. A layer of simple squamous epithelium is attached to the periosteum of the bone surrounding each of these chambers. The wall of the membranous labyrinth that bounds the scala vestibuli is called the vestibular membrane (Reissner’s membrane); the wall of the membranous labyrinth bordering the scala tympani is the basilar membrane. The space between the vestibular membrane and the basilar membrane is the interior of the membranous labyrinth and is called the cochlear duct or scala media, which is .lled with endolymph. The vestibular membrane consists of a double layer of squamous epithelium and is the simplest region of the membranous labyrinth. The vestibular membrane is so thin that it has little or no mechanical effect on the transmission of sound waves through the inner ear; therefore, the perilymph and endolymph on the two sides of the vestibular membrane can be thought of mechanically as one .uid. The role of the vestibular membrane is to separate the two chemically different .uids. The basilar membrane is somewhat more complex and is of much greater physiologic interest in relation to the mechanics of hearing. It consists of an acellular portion with collagen .bers, ground substance, and sparsely dispersed elastic elastic .bers and a cellular part with a thin layer of vascular connective tissue that is overlaid with simple squamous epithelium. The basilar membrane is attached at one side to the bony spiral lamina, which projects from the sides of the modiolus, the bony core of the cochlea, like the threads of a screw, and at the other side to the lateral wall of the bony labyrinth by the spiral ligament, a local thickening of the periosteum. The distance between the spiral lamina and the spiral ligament increases from 0.04 mm near the oval window to 0.5 mm near the helicotrema. The collagen .bers of the basilar membrane are oriented across the membrane between the spiral lamina and the spiral ligament, somewhat like the strings of a piano. The collagen .bers near the oval window are both shorter and thicker than those near the helicotrema. The diameter of the collagen .bers in the membrane decreases as the basilar membrane widens. As a result, the basilar membrane near the oval window is short and stiff, and responds to high-frequency vibrations, whereas that part near the helicotrema is wide and limber and responds to low-frequency vibrations.

The cells inside the cochlear duct are highly modi.ed to form a structure called the spiral organ, or the organ of Corti. The spiral organ contains supporting epithelial cells and specialized sensory cells called hair cells, which have hairlike projections at their apical ends. In children, these projections consist of one cilium (kinocilium) and about 80 very long microvilli, often referred to as stereocilia; but in adults the cilium is absent from most hair cells. The hair cells are arranged in four long rows extending the length of the cochlear duct. The tips of the hairs are embedded within an acellular gelatinous shelf called the tectorial membrane, which is attached to the spiral lamina.

Hair cells have no axons, but the basilar regions of each hair cell are covered by synaptic terminals of sensory neurons, the cell bodies of which are located within the cochlear modiolus and are grouped into a cochlear, or spiral ganglion. Afferent .bers of these neurons join to form the cochlear nerve. This nerve then joins the vestibular nerve to become the vestibulocochlear nerve (VIII), which traverses the internal auditory meatus and enters the cranial vault.

(a) Each sound wave consists of a region of compressed air between two regions of less compressed air (blue bars). The sigmoid waves correspond to the regions of more compressed air (peaks) and less compressed air (troughs). The green shadowed area represents the width of one cycle (distance between peaks). When something like a tuning fork or vocal cords vibrate, the movements of the object alternate between compressing the air and decompressing the air, or making the air less compressed, thus producing sound.

(b) Depicts low- and high-volume sound waves. Compare the relative lengths of the arrows indicating the wave height (amplitude).

(c) Depicts lower and higher pitch sound. Compare the relative number of peaks (frequency) within a given time interval (between arrows).

 

Mechanism of conduction of sound waves

1.                 Sound waves strike tympanic membrane. Ossicular system conducts this sound. Faceplate of stapes moves inward into scala media at oval window. So fluid moves inward into scala media. It causes vibration of basilar membrane. When basilar membrane bends upward to scala vestibuli, hair cells depolarize and generate action potential to nerve fibers of cochlear nerve.

2.                 Place principle determines sound frequency by determining the position along basilar membrane that it most stimulated. Low frequency sounds cause maximal stimulation of basilar membrane near apex of cochlear. High frequency sounds cause maximal stimulation of basilar membrane near base of cochlear.  Intermediate frequency sounds cause maximal stimulation of basilar membrane at middle of cochlear.

As the stapes vibrates, it produces waves in the perilymph of the scala vestibuli. Vibrations of the perilymph are transmitted through the thin vestibular membrane and cause simultaneous vibrations of the endolymph. The mechanical effect is as though the perilymph and endolymph were a single fluid. Vibration of the endolymph causes distortion of the basilar membrane. Waves in the perilymph of the scala vestibuli are transmitted also through the helicotrema and into the scala tympani. Because the helicotrema is very small, however, this transmitted vibration is probably of little consequence. Distortions of the basilar membrane, together with weaker waves coming through the helicotrema, cause waves in the scala tympani perilymph and ultimately result in vibration of the membrane of the round window.

Vibration of the round window membrane is important to hearing because it acts as a mechanical release for waves from within the cochlea. If this window were solid, it would re.ect the waves, which would interfere with and dampen later waves. The round window also allows relief of pressure in the perilymph because fluid is not compressible, thereby preventing compression damage to the spiral organ.

The distortion of the basilar membrane is most important to hearing. As this membrane distorts, the hair cells resting on the basilar membrane move relative to the tectorial membrane, which remains stationary. The hair cell microvilli, which are embedded in the tectorial membrane, become bent, causing depolarization of the hair cells. The hair cells then induce action potentials in the cochlear neurons that synapse on the hair cells, apparently by direct electrical excitation through electrical synapses rather than by neurotransmitters.

The hairs of the hair cells are bathed in endolymph. Because of the difference in the potassium and sodium ion concentrations between the perilymph and endolymph, an approximately 80 mV potential exists across the vestibular membrane between the two .uids. This is called the endocochlear potential. Because the hair cell hairs are surrounded by endolymph, the hairs have a greater electric potential than if they were surrounded by perilymph. It’s believed that this potential difference makes the hair cells much more sensitive to slight movement than they would be if surrounded by perilymph.

The part of the basilar membrane that distorts as a result of endolymph vibration depends on the pitch of the sound that created the vibration and, as a result, on the vibration frequency within the endolymph. The width of the basilar membrane and the length and diameter of the collagen .bers stretching across the membrane at each level along the cochlear duct determine the location of the optimum amount of basilar membrane vibration produced by a given pitch. Higher-pitched tones cause optimal vibration near the base, and lower-pitched tones cause optimal vibration near the apex of the basilar membrane. As the basilar membrane vibrates, hair cells along a large part of the basilar membrane are stimulated. In areas of minimum vibration, the amount of stimulation may not reach threshold. In other areas, a low frequency of afferent action potentials may be transmitted, whereas in the optimally vibrating regions of the basilar membrane, a high frequency of action potentials is initiated.

 

Determination of loudness of sounds

   There are three ways for determination of loudness of sounds during its perception. As sound becomes louder, amplitude of vibrations of basilar membrane increases. so hair cells produce impulses at rapid rate.

   Increase of sound amplitude cause rise of quantity of excited hair cells. Loud sound stimulates also special high-threshold hair cells, which appraise the central nervous system, that sound is loud.

Effect of Sound Waves on Points Along the Basilar Membrane

Points of maximum vibration along the basilar membrane resulting from stimulation by sounds of various frequencies (in hertz).

 

The Ear Pages, consisting of readings, animations and quizes, is based on the 1961 Nobel Prize in Physiology or Medicine, which was awarded for the discovery of how sound is analyzed and communicated in the cochlea in the inner ear.

The Ear Pages

Central division of auditory analyzer

•         Hair cells are secondary sensitive cells, which give receptor potential to neurons of spiral ganglion of Corti. Then impulse puss to vestibulocochlear nerve - dorsal and ventral cochlear nuclei in upper medulla - trapezoid body - superior olivary nucleus - lateral lemniscus. Then fibers divide into three parts, which go to:

•         - nucleus of lateral lemniscus;

•         - higher centers;

•         - inferior colliculi - medial geniculate nucleus - auditory cortex through auditory radiation.

•         Auditory cortex lies in superior gyrus of temporal lobe and performs final processing of auditory information.

 

Neuronal Pathways for Hearing

The special senses of hearing and balance are both transmitted by the vestibulocochlear (VIII) nerve. The term vestibular refers to the vestibule of the inner ear, which is involved in balance. The term cochlear refers to the cochlea and is that portion of the inner ear involved in hearing. The vestibulocochlear nerve functions as two separate nerves carrying information from two separate but closely related structures.

The auditory pathways within the CNS are very complex, with both crossed and uncrossed tracts. Unilateral CNS damage therefore usually has little effect on hearing. The neurons from the cochlear ganglion synapse with CNS neurons in the dorsal or ventral cochlear nucleus in the superior medulla near the inferior cerebellar peduncle. These neurons in turn either synapse in or pass through the superior olivary nucleus.

Neurons terminating in this nucleus may synapse with efferent neurons returning to the cochlea to modulate pitch perception. Nerve .bers from the superior olivary nucleus also project to the trigeminal (V) nucleus, which controls the tensor tympani, and the facial (VII) nucleus, which controls the stapedius muscle. This re.ex pathway dampens loud sounds by initiating contractions of these muscles. This is the sound attenuation re.ex described previously. Neurons synapsing in the superior olivary nucleus may also join other ascending neurons to the cerebral cortex.

Ascending neurons from the superior olivary nucleus travel in the lateral lemniscus. All ascending fibers synapse in the inferior colliculi, and neurons from there project to the medial geniculate nucleus of the thalamus, where they synapse with neurons that project to the cortex. These neurons terminate in the auditory cortex in the dorsal portion of the temporal lobe within the lateral fissure and, to a lesser extent, on the superolateral surface of the temporal lobe (see chapter 13). Neurons from the inferior colliculus also project to the superior colliculus, where re.exes that turn the head and eyes in response to loud sounds are initiated.

Binaural hearing

•         Binaural hearing helps in determination of direction to sound origin. Binaural hearing provides detection of time-lag between entry of sound into one ear and into opposite ear. Medial superior olivary nucleus detects this information.

•         Difference between intensities of sound in two ears also is important for determination of direction to sound origin. Lateral superior olivary nucleus detects it.

Vestibular analyzer

Functions of vestibular analyzer

•        It is analyzer system, which detects sensation concerned with equilibrium and determines normal orientation and body movement with respect to direction of gravity power or acceleratory forces.

•        Information from vestibular analyzer helps in proper autonomic and metabolic control of skeletal muscles, which support proper locomotion and body posture under the influence of Earth Gravity power.

Peripheral division of vestibular analyzer

•        It is located in bony tubes and chambers in petrose portion of temporal bone. Membranous labyrinth is a system of soft tissue tubes and chambers filling within bony labyrinth.

•        There are three semicircular canals ant two chambers, i.e. utricle and sacule, which are filled with endolymph

 Balance

The organs of balance are divided structurally and functionally into two parts. The .rst, the static labyrinth, consists of the utricle and saccule of the vestibule and is primarily involved in evaluating the position of the head relative to gravity, although the system also responds to linear acceleration or deceleration, such as when a person is in a car that is increasing or decreasing speed. The second, the kinetic labyrinth, is associated with the semicircular canals and is involved in evaluating movements of the head.

Most of the utricular and saccular walls consist of simple cuboidal epithelium. The utricle and saccule, however, each contain a specialized patch of epithelium about 2–3 mm in diameter called the macula. The macula of the utricle is oriented parallel to the base of the skull, and the macula of the saccule is perpendicular to the base of the skull. The maculae resemble the spiral organ and consist of columnar supporting cells and hair cells. The “hairs”of these cells, which consist of numerous microvilli, called stereocilia, and one cilium, called a kinocilium, are embedded in a gelatinous mass weighted by the presence of otoliths composed of protein and calcium carbonate. The gelatinous mass moves in response to gravity, bending the hair cells and initiating action potentials in the associated neurons. De.ection of the hairs toward the kinocilium results in depolarization of the hair cell, whereas defiection of the hairs away from the kinocilium results in hyperpolarization of the hair cell. If the head is tipped, otoliths move in response to gravity and stimulate certain hair cells. The hair cells are constantly being stimulated at a low level by the presence of the otolith-weighted covering of the macula; but as this covering moves in response to gravity, the pattern of intensity of hair cell stimulation changes. This pattern of stimulation and the subsequent pattern of action potentials from the numerous hair cells of the maculae can be translated by the brain into speci.c information about head position or acceleration.Much of this information is not perceived consciously but is dealt with subconsciously. The body responds by making subtle tone adjustments in muscles of the back and neck,which are intended to restore the head to its proper neutral, balanced position.

The kinetic labyrinth consists of three semicircular canals placed at nearly right angles to one another, one lying nearly in the transverse plane, one in the coronal plane, and one in the sagittal plane. The arrangement of the semicircular canals enables a person to detect movement in all directions. The base of each semicircular canal is expanded into an ampulla.Within each ampulla, the epithelium is specialized to form a crista ampullaris. This specialized sensory epithelium is structurally and functionally very similar to that of the maculae. Each crista consists of a ridge or crest of epithelium with a curved gelatinous mass, the cupula, suspended over the crest. The hairlike processes of the crista hair cells, similar to those in the maculae, are embedded in the cupula.

The cupula contains no otoliths and therefore doesn’t respond to gravitational pull. Instead, the cupula is a .oat that is displaced by .uid movements within the semicircular canals. Endolymph movement within each semicircular canal moves the cupula, bends the hairs, and initiates action potentials.

As the head begins to move in a given direction, the endolymph does not move at the same rate as the semicircular canals. This difference causes displacement of the cupula in a direction opposite to that of the movement of the head, resulting in relative movement between the cupula and the endolymph. As movement continues, the .uid of the semicircular canals begins to move and “catches up” with the cupula, and stimulation is stopped. As movement of the head ceases, the endolymph continues to move because of its momentum, causing displacement of the cupula in the same direction as the head had been moving. Because displacement of the cupula is most intense when the rate of head movement changes, this system detects changes in the rate of movement rather than movement alone. As with the static labyrinth, the information obtained by the brain from the kinetic labyrinth is largely subconscious.

 

Utricle and saccule function

•        Macula is sensory organ of utricle and saccule. It is covered with gelatinous layer. Cilia of hair cells lay there. Hair cells synapse with sensory axons of vestibular nerve. Macula of utricle determines normal orientation of willi respect to direction of gravitational or acceleratory forces.

•        Macula of sacule detects certain tips of sounds and detects equilibrium when head is not in vertical position. In the beginning or end of linear motion of the head or whole the body, otolith membrane moves because of its inertion. So, irritation of sensory hair cells occurs.

Semicircular canal function

•        Ampula is enlargement at one end of semicircular canal. It has a small crest on top of which is a gelatinous mass known as cupula. Hair cells have two kinds of cilia – kinocilium and stereocilia.

•        Kinocilium is large cilium located at one end of hair cell. Stereocilia are small. When stereocilia are bent towards kinocilium, hair cell is depolarized, i.e. stimulated.

 

Semicircular Canals

(a) Semicircular canals showing location of the crista ampullaris in the ampullae of the semicircular canals.

(b) Enlargement of the crista ampullaris, showing the cupula and hair cells.

(c) Enlargement of a hair cell.

Function of the Semicircular Canals

The crista ampullaris responds to .uid movements within the semicircular canals. (a) When a person is at rest, the crista ampullaris does not move.

(b) As a person begins to move in a given direction, the semicircular canals begin to move with the body (blue arrow), but the endolymph tends to remain stationary relative to the movement (momentum force: red arrow pointing in the opposite direction of body and semicircular canal movement), and the crista ampullaris is displaced by the endolymph in a direction opposite to the direction of movement.

Conductive and central division of vestibular analyzer

•        Hair sensory cells give impuls to vestibulocochlear nerve, vestibular nuclei and uvula and flocculonodular lobe. Superior and medial vestibular nuclei cause corrective movements of eyes and appropriate movements of head and neck.

•        Lateral vestibular nucleus controls body movements. Inferior vestibular nucleus sends signals to cerebellum and reticular formation.

Vestibulosomatic reactions

•        These are reactions of skeletal musculature as a result of irritation of vestibular sensory organs. Vestibulosomatic reactions are presented by distribution of muscle tone through the body, general motor reactions or eyeball movements.

•        In case of assuasive or unusual vestibular stimulation rapid uneven movements of both eyeballs occur. This is nystagmus.

•        If head is rotated to left, eyes move towards right in order to prevent image from moving off fovea. When eyes have rotated as far as they can, they are rapidly returned to center of socket. If rotation of head continues, eyes move in direction opposite to head rotation.

Neuronal Pathways for Balance

Neurons synapsing on the hair cells of the maculae and cristae ampullares converge into the vestibular ganglion, where their cell bodies are located. Sensory .bers from these neurons join sensory .bers from the cochlear ganglion to form the vestibulocochlear nerve (VIII) and terminate in the vestibular nucleus within the medulla oblongata. Axons run from this nucleus to numerous areas of the CNS, such as the spinal cord, cerebellum, cerebral cortex, and the nuclei controlling extrinsic eye muscles.

Balance is a complex process not simply con.ned to one type of input. In addition to vestibular sensory input, the vestibular nucleus receives input from proprioceptive neurons throughout the body, and from the visual system. People are asked to close their eyes while balance is evaluated in a sobriety test because alcohol affects the proprioceptive and vestibular components of balance (cerebellar function) to a greater extent than it does the visual portion.

Reflex pathways exist between the kinetic part of the vestibular system and the nuclei controlling the extrinsic eye muscles (oculomotor, trochlear, and abducens). A reflex pathway allows maintenance of visual .xation on an object while the head is in motion. This function can be demonstrated by spinning a person around about 10 times in 20 seconds, stopping him or her, and observing eye movements. The reaction is most pronounced if the individual’s head is tilted forward about 30 degrees while spinning, thus bringing the lateral semicircular canals into the horizontal plane. A slight oscillatory movement of the eyes occurs. The eyes track in the direction of motion and return with a rapid recovery movement before repeating the tracking motion. This oscillation of the eyes is called nystagmus. If asked to walk in a straight line, the individual deviates in the direction of rotation, and if asked to point to an object, his or her .nger deviates in the direction of rotation.

Vestibuloautonomic reactions

•         Diverging of impulses to autonomic subcortical nuclei is necessary for proper distribution of blood supply and metabolic activity between visceral organs and contracting muscles.

•         Inadequate stimulation of vestibular receptors lead to improper autonomic stimulation, which may result in changing of heart beat rate, arterial pressure, motoric of digestive tract so on.

Age peculiarities of vestibular sensory system

•         Until the moment of birth human has vestibular analyzer system developed well. All the conductive pathways are mielinised.

•         Vestibular reactivity has genetic basis and could not be changed considerably through the life.

 Somatic sensory analyzer

 Touch

Our sense of touch is actually four senses—pressure, warmth, cold, and pain—that combine to produce other sensations, such as "hot." One theory of pain is that a "gate" in the spinal cord either opens to permit pain signals traveling up small nerve fibers to reach the brain, or closes to prevent their passage. Because pain is both a physiological and a psychological phenomenon, it often can be controlled through a combination of physical and psychological treatments.

While vision, hearing, smell, and taste provide you with important information about your environment, another group of senses provides you with information that comes from a source much closer to home: your own body. In this section, we’ll first consider the skin senses, which provide essential information about your physical status and your physical interaction with objects in your environment. We’ll next consider the body senses, which keep you informed as to your position and orientation in space. own body. In this section, we’ll first consider the skin senses, which provide essential information about your physical status and your physical interaction with objects in your environment.

We’ll next consider the body senses, which keep you informed as to your position and orientation in space. We usually don’t think of our skin as a sense organ. But the skin is in fact the largest and heaviest sense organ. The skin of an average adult covers about 20 square feet of surface area and weighs about six pounds. There are many different kinds of sensory receptors in the skin. Some of these sensory receptors are specialized to respond to just one kind of stimulus, such as pressure, warmth, or cold. Other skin receptors respond to more than one type of stimulus.

One important receptor involved with the sense of touch, called the Pacinian corpuscle, is located beneath the skin. When stimulated by pressure, the Pacinian corpuscle converts the stimulation into a neural message that is relayed to the brain. If a pressure is constant, sensory adaptation takes place. The Pacinian corpuscle either reduces the number of signals sent or quits responding altogether (which is fortunate, or you’d be unable to forget the fact that you’re wearing underwear). Sensory receptors are distributed unevenly among different areas of the body, which is why sensitivity to touch and temperature varies from one area of the body to another. Your hands, face, and lips, for example, are much more sensitive to touch than are your back, arms, and legs. That’s because your hands, face, and lips are much more densely packed with sensory receptors.

 

 

 

Body Position and Movement

Finally, our effective functioning requires a kinesthetic sense, which notifies the brain of the position and movement of body parts, and a sense of equilibrium, which monitors the position and movement of the whole body.

 Pain begins when an intense stimulus activates small-diameter sensory fibers, called free nerve endings, in the skin, muscles, or internal organs. The free nerve endings carry their messages to the spinal cord, releasing a neurotransmitter called substance P. In the spinal cord, substance P causes other neurons to become activated, sending their messages through open spinal gates to the thalamus in the brain (Turk & Nash, 1993). Other areas of the brain involved in the experience of pain are the somatosensory cortex and areas in the frontal lobes and limbic system that are involved in emotion (Hunt & Mantyh, 2001; Rainville & others, 1997). When the sensory pain signals reach the brain, the sensory information is integrated with psychological information. Depending on how the brain interprets the pain experience, it regulates pain by sending signals down the spinal cord that either open or close the gates. If, because of psychological factors, the brain signals the gates to open, pain is experienced or intensified. If the brain signals the gates to close, pain is reduced.

Anxiety, fear, and a sense of helplessness are some of the psychological factors that can intensify the experience of pain. Positive emotions, laughter, distraction, and a sense of control can reduce the perception of pain. The experience of pain is also influenced by social and cultural learning experiences about the meaning of pain and how people should react to pain (Turk, 1994; Turk & Rudy, 1992). Psychological factors also influence the release of endorphins, the body’s natural painkillers that are produced in many parts of the brain and the body. Endorphins are released as part of the brain’s overall response to physical pain or stress. In the brain, endorphins can inhibit the transmission of pain signals. In the spinal cord, endorphins inhibit the release of substance P. Finally, a person’s mental or emotional state can influence other bodily processes that affect the experience of pain. Muscle tension, psychological arousal, and rapid heart rate can all produce or intensify pain (Turk & Nash, 1993). Today, a variety of techniques and procedures can effectively eliminate or reduce pain.

 

Movement, Position, and Balance

The phone rings. Without looking up from your textbook, you reach for the receiver, pick it up, and guide it to the side of your head. You have just demonstrated your kinesthetic sense—the sense that involves the location and position of body parts in relation to one another. (The word

kinesthetics literally means “feelings of motion.”) The kinesthetic sense involves specialized sensory neurons, called proprioceptors, which are located in the muscles and joints. The proprioceptors constantly communicate information to the brain about changes in body position and muscle tension. Closely related to the kinesthetic sense is the vestibular sense, which provides a sense of balance, or equilibrium, by responding to changes in gravity, motion, and body position. The two sources of vestibular sensory information, the semicircular canals and the vestibular sacs, are both located in the ear. These structures are filled with fluid and lined with hairlike receptor cells that shift in response to motion, changes in body position, or changes in gravity. When you experience environmental motion, like the rocking of a boat in choppy water, the fluids in the semicircular canals and the vestibular sacs are affected. Changes in your body’s position, such as falling backward in a heroic attempt to return a volleyball serve, also affect the fluids. Your vestibular sense supplies the critical information that allows you to compensate for such changes and quickly reestablish your sense of balance.

Maintaining equilibrium also involves information from other senses, particularly vision. Under normal circumstances, this works to our advantage. However, when information from the eyes conflicts with information from the vestibular system, the result can be dizziness, disorientation, and nausea. These are the symptoms commonly experienced in motion sickness, the bane of many travelers in cars, on planes, on boats, and even in space. One strategy that can be used to combat motion sickness is to minimize sensory conflicts by focusing on a distant point or an object that is fixed, such as the horizon.

In the first part of this chapter, we’ve described how the body’s senses respond to stimuli in the environment. Table 3.4 summarizes these different sensory systems. To make use of this raw sensory data, the brain must organize and interpret the data and relate it to existing knowledge. Next, we’ll look at the process of perception—how we make sense out of the information that we receive from our environment.

proprioception How do you know where your fingers are, or how much force your muscles are exerting? The terms proprioception and kinaesthesia cover these sensations. The terms were coined in the late nineteenth century, and evolved to be synonyms, despite their different historical backgrounds. They refer to neural signals which have access to consciousness and which can contribute to controlling the movement and posture of the body. These signals arise from peripheral sensors and from internally generated ‘commands’ to move. The former arise from inputs to the central nervous system from specialized receptors, which respond to forces and length changes in muscles, joints, and ligaments, and in the skin. Not surprisingly, all these classes of specialized receptors can change their discharge during voluntary movement and muscle contractions. This finding has been confirmed in conscious human volunteers by recording the discharge of single nerve fibres from these receptors with a microelectrode inserted into a peripheral nerve. This technique is termed microneurography. Perceived signals of ‘motor commands’ arise within the brain and are related to the timing and effort involved in deliberate muscular contractions.

Proprioception is not a single sensation but a group of sensations. It includes the sensations of position and movement of joints (loosely termed ‘joint position sense’ by neurologists), sensations of muscular force and effort, sensations related to the perceived timing of contractions, and sensations related to the body image. As well as this diversity in the various sensations making up proprioception, even for an individual component more than one mechanism can operate. From an evolutionary point of view this redundancy is not surprising: it ensures that crucial elements in the control of movement are not dependent on a single channel of information.

Clinicians frequently assess a patient's sensation of passive movement of a joint. If it is unimpaired, they then know that some peripheral receptors, their links to the spinal cord via peripheral nerves, and their ascending pathways to the thalamus and then to specialized regions of the cerebral cortex, are all intact. Controversy has dogged understanding of this aspect of proprioception, because researchers have often emphasized the role of one category of input and appeared to deny the role of other inputs. However, it is now clear that input from muscle, joint, and skin receptors can provide perceived signals that joints have moved, and in which direction.

Signals from the sensory endings within the main receptors in muscles, the muscle spindles, probably play an important role in signalling the direction of passive movements and their velocity. Muscle spindle endings respond to very small changes in muscle length, and the gain of their input can be affected by the specialized motor output from the spinal cord to the spindles, termed the fusimotor system. Specific signals from muscle spindle endings are interpreted centrally in the light of the fusimotor output to them, along with signals from antagonist muscles, joints, and nearby skin. Most joint receptors discharge towards the extreme end of a range of movement, while some local and more remote cutaneous receptors discharge as the skin is distorted by movement of nearby joints.

The force of a muscle contraction, and the apparent heaviness of weights actively lifted by the limb, are encoded by sensitive tension receptors (Golgi tendon organs). They are connected between the muscle fibres and intramuscular extensions of the tendon, and they respond to global forces generated actively by the muscle. However, a potent additional mechanism dominates judgements about force and heaviness: signals of motor command or effort are critical. An abnormal increase in motor command or effort can explain why weights lifted by fatigued or pathologically weakened muscles feel heavy despite the fact that their physical weight is unchanged. In an experimental situation subjects can distinguish between the signals of central command and those of peripheral force. However, this distinction is less obvious when lifting a heavy suitcase at an airport — it still seems to get heavier.
For the various sensations comprising proprioception, acuity is not necessarily identical at all joints of the body. As examples, detection of passive movements applied to the terminal joint of the big toe over a range of velocities is comparatively poor, while, for judgements of force, accuracy is comparatively high across a wide range of forces for the terminal joint of the thumb.
Rather like the judgements of force, the proprioceptive mechanisms that determine the perceived timing of muscle contractions have both a ‘peripheral’ and a ‘central’ component. Subjects can attend to either a central signal associated with the motor command to move, or one arising from muscle, joint, and skin receptors after the muscle contraction has begun. Clearly the former signal is generated without a peripheral input, because it arises before movement occurs. Furthermore, subjects can accurately attend to signals about the size and destination of motor commands, particularly those directed to the intrinsic muscles which move the fingers and thumb.
The importance of input from proprioceptors is highlighted when peripheral nerve damage (such as a severe sensory neuropathy), or damage within the brain (such as a stroke), eliminates sensations based on signals from specialized muscle, joint, and cutaneous receptors. When this occurs there is marked impairment of tasks requiring manipulative skill and the co-ordination of multiple muscle groups, such as walking. It also becomes difficult to sustain a steady muscle contraction. More restricted losses of proprioceptive inputs, such as those following surgical replacement of joints, produce only minor impairment to proprioception.

Role of proprioception

sensory receptors of several kinds are involved in the complex process of maintaining uprightness, as well as in the recognition of the imminence of toppling. There are no ‘gravity receptors’ as such, in spite of what is generally believed. The parts of the inner ear commonly associated with this function turn out to be accelerometers; i.e. they are detectors of stress gradient, not of gravity. Proprioceptors elsewhere in the body can also act as accelerometers and thus make a contribution to indicating the direction of the resultant support thrust. The actual position of the thrust line is indicated by deformation of the soft tissues of the feet and hands at the areas of contact with the supports. Movements of the head during overbalancing are indicated by the streaming of details in the images of the environment on the peripheral retina.

Stability

Restricting the area of support diminishes the available range through which the support thrust can be moved to resist perturbations, unless the position of the support is itself appropriately moved by the perturbation. When an egg is placed on a hard surface, the area of support is restricted to the very small area of contact. It is, accordingly, very hard to balance an egg on one end, because any accidental tilting produces more movement of the c of g than of the point of support, the centre of curvature of the shell at the ends being below the c of g of the egg. The shift of the thrust line, which necessarily passes through the area of support, is thus not sufficient to correct the tilt. With the egg on its side, however, a brief push in the direction of the long axis of the egg produces temporary rocking, followed by a return to the original position. The centre of curvature in the plane of the long axis is above the c of g, so the shift of the thrust line exceeds that of the c of g. For a sideways perturbation, the centre of curvature is coincident with the c of g, and the egg just rolls away from the perturbation, with the thrust line continuing to pass through the c of g. This is what happens to a wheel: the balance is neither stable nor unstable.

If the body of an animal or of a person is to stay in more or less the same place, any accidental displacement in a particular direction will have to be corrected by a corresponding displacement in the opposite direction. This is achieved by adjusting, by muscular forces, the thrust forces exerted by the limbs against the supports — in magnitude, in direction, in timing, and in point of application.

Anticipatory pre-emptive actions

A number of reflex reactions have been identified that produce the appropriate changes in the musculature, by swaying, hopping, and stepping. In the intact subject, however, many of these reflexes are effectively replaced by ‘anticipatory pre-emptive actions’. These are voluntary actions, based on the underlying reflexes, but initiated in response to the detection that the incoming sensory information is changing in a way that might lead to a need for corrective action. Appropriate action is initiated early, before the reflex responses themselves are triggered into action. Frequent rehearsal, from a very early age, leads to these voluntary actions being performed without the subject being aware of what is going on—that is to say, they become habits. Their promptness plays an important role in maintaining smoothness of control, since they are not subject to the delays inevitable in reflex responses.

Overbalancing

The erect posture of man, particularly when standing on one leg, is a condition of precarious equilibrium, because the area of support is small compared with the height of the c of g above the feet. The strategies for avoiding falling over are related to what happens to an egg placed on its side. Small perturbations are met by shifting the centre of pressure at the foot and thus developing an inclined thrust to oppose the perturbation, as in the egg displaced in the direction of its long axis. This strategy will fail when the thrust line reaches the edge of the area of support, because further displacement will cause the body to topple. The imminence of such toppling is detected by the proprioceptive system and a different strategy is brought into play. If another limb is available, it will be thrust out in the direction of the impending fall in a ‘rescue reaction’ that attempts to find a firm obstacle against which to develop force and thus to extend the effective area of support. This is the basis of stepping. A succession of steps, in locomotion, brings the legs into action in turn, like the spokes of a wheel, so that the body may be moved through an indefinite distance without falling over—like the egg being rolled sideways. The legs do not provide the same continuous support as a wheel because, when one leg is being swung forward in a step, the body topples forward over the stance leg and acquires some downward momentum. This toppling movement has to be corrected when the swing leg eventually touches down, so this leg then at first gives, to absorb the unwanted momentum, and later straightens again to restore the c of g to its earlier height above the ground. As the body continues to move forward over the new stance foot, that leg extends to provide extra thrust, which propels the body forward into the next step. If this thrust is strong enough, the body can be launched into a free fall phase while the free leg is still swinging. This extends the step length, as in running or jumping.

Uprightness

When an object is at rest on a stationary support, the thrust line is parallel to a radius of the planet, i.e. it lies in the gravitational vertical. Experiments with moving platforms reveal, however, that the direction of the thrust line appropriate to the avoidance of falling over is dependent on the accelerations associated with the movement of the platform. A person standing in a vehicle that is moving in a curved path has to lean inwards, to develop a horizontal component of thrust to accelerate his body into an equally curved path, as well as developing an upward thrust to prevent falling. The best direction for the thrust line is thus not the same as the gravitational vertical.

 

The thrust developed against the supports, both on moving platforms and on firm ground, is under continuous readjustment by the nervous system to suit the needs of the moment, be it to remain in one place or to move about in locomotion or athletic activity. The successful control of the necessary muscular activity is a matter of skill; the basis of this is first acquired in infancy and it is continually being revised and rehearsed throughout life as different types of activity are undertaken.

(T. D. M. Roberts Bibliography Roberts, T. D. M. (1995) Understanding Balance, Chapman and Hall, London._

Taste

Taste, a chemical sense, is likewise a composite of five basic sensations—sweet, sour, salty, bitter, and umami—and of the aromas that interact with information from the taste buds. The influence of smell on our sense of taste is an example of sensory interaction.

Our sense of taste, or gustation, results from the stimulation of special receptors in the mouth. The stimuli that produce the sensation of taste are chemical substances in whatever you eat or drink. These substances are dissolved by saliva, allowing the chemicals to activate the taste buds. Each taste bud contains about 50 receptor cells that are specialized for taste.

 

(a) Surface of the tongue

(b) Filiform papillae

(c) Vallate papillae

(d) Foliate papillae

(e) Fungiform papillae

(f) A taste bud

(g) Scanning electron micrograph of taste buds (fungiform and filiform papillae) on the surface of the tongue.

 

The surface of the tongue is covered with thousands of little bumps with grooves in between. These grooves are lined with the taste buds. Taste buds are also located on the insides of your cheeks, on the roof of your mouth, and in your throat (Oakley, 1986). When activated, special receptor cells in the taste buds send neural messages along pathways to the thalamus in the brain. In turn, the thalamus directs the information to several regions in the cortex (O’Doherty & others, 2001b). There were long thought to be four basic taste categories: sweet, salty, sour, and bitter. Recently, the receptor cells for a fifth basic taste, umami, were identified (Chaudhari & others, 2000). Loosely translated, umami means “yummy” or “delicious” in Japanese. Umami is the distinctive taste of monosodium glutamate and is associated with protein-rich foods and the savory flavor of Parmesan and other aged cheeses, mushrooms, seaweed, and meat. Each taste bud shows maximum sensitivity to one particular taste, and lesser sensitivity to other tastes. Most tastes are complex and result from the activation of different combinations of basic taste receptors. Taste is just one aspect of flavor, which involves several sensations, including the aroma, temperature, texture, and appearance of food.

The sensory structures that detect gustatory, or taste, stimuli are the taste buds. Most taste buds are associated with specialized portions of the tongue called papillae. Taste buds, however, are also located on other areas of the tongue, the palate, and even the lips and throat, especially in children. The four major types of papillae are named according to their shape: vallate, fungiform, foliate, and filiform. Taste buds are associated with vallate, fungiform, and foliate papillae. Filiform papillae are the most numerous papillae on the surface of the tongue but have no taste buds.

Vallate papillae are the largest but least numerous of the papillae. Eight to 12 of these papillae form a V-shaped row along the border between the anterior and posterior parts of the tongue. Fungiform papillae are scattered irregularly over the entire superior surface of the tongue and appear as small red dots interspersed among the far more numerous filiform papillae. Foliate papillae are distributed in folds on the sides of the tongue and contain the most sensitive of the taste buds. They are most numerous in young children and decrease with age. They are located mostly posteriorly in adults.

Histology of Taste Buds

Taste buds are oval structures embedded in the epithelium of the tongue and mouth. Each of the 10,000 taste buds on a person’s tongue consists of two types of specialized epithelial cells. One type forms the exterior supporting capsule of the taste bud, whereas the interior of each bud consists of about 50 taste or gustatory cells. Like olfactory cells, cells of the taste buds are replaced continuously, each having a normal life span of about 10 days. Each taste cell has several microvilli, called gustatory hairs, extending from its apex into a tiny opening in the epithelium called the taste or gustatory pore.

Function of Taste

Substances called tastants, dissolved in saliva, enter the taste pore and, by various mechanisms, cause the taste cells to depolarize. These cells have no axons and don’t generate their own action potentials. Neurotransmitters are released from the taste cells and stimulate action potentials in the axons of sensory neurons associated with them.

The taste of salt results when Na+ diffuse through Na+ channels of the gustatory hairs or other cell surfaces of taste cells, resulting in depolarization of the cells. Hydrogen ions (H+) of acids can cause depolarization of taste cells by one of three

mechanisms: (1) they can enter the cell directly through H+ channels, (2) they can bind to ligand-gated K+ channels and block the exit of K+ from the cell, or (3) they can open ligand-gated channels for other positive ions and allow them to diffuse into the cell. Sweet and bitter tastants bind to receptors on the gustatory hairs of taste cells and cause depolarization through a G protein mechanism. A new taste, called umami by the Japanese, results when amino acids, such as glutamate, bind to receptors on gustatory hairs of taste cells and cause depolarization through a G protein mechanism.

The texture of food in the oral cavity also affects the perception of taste. Hot or cold food temperatures may interfere with the ability of the taste buds to function in tasting food. If a cold .uid is held in the mouth, the .uid becomes warmed by the body, and the taste becomes enhanced. On the other hand, adaptation is very rapid for taste. This adaptation apparently occurs both at the level of the taste bud and within the CNS. Adaptation may begin within 1 or 2 seconds after a taste sensation is perceived, and complete adaptation may occur within 5 minutes. Even though only .ve primary tastes have been identi.ed, humans can perceive a fairly large number of different tastes, presumably by combining the basic taste sensations. As with olfaction, the speci.city of the receptor molecules is not perfect. For example, artificial sweeteners have different chemical structures than the sugars they are designed to replace and are often many times more powerful than natural sugars in stimulating taste sensations. Many of the sensations thought of as being taste are strongly influenced by olfactory sensations. This phenomenon can be demonstrated by pinching one’s nose to close the nasal passages, while trying to taste something. With olfaction blocked, it’s dif.cult to distinguish between the taste of a piece of apple and a piece of potato. Much of the “taste” is lost by this action.

Actions of the Major Tastants

 

Although all taste buds are able to detect all .ve of the basic tastes, each taste cell is usually most sensitive to one. Thresholds vary for the .ve primary tastes. Sensitivity for bitter substances is the highest; sensitivities for sweet and salty tastes are the lowest. Sugars, some other carbohydrates, and some proteins produce sweet tastes; many proteins and amino acids produce umami tastes; acids produce sour tastes; metal ions tend to produce salty tastes; and alkaloids (bases) produce bitter tastes. Many alkaloids are poisonous; thus the high sensitivity for bitter tastes may be protective. On the other hand, humans tend to crave sweet, salty, and umami tastes, perhaps in response to the body’s need for sugars, carbohydrates, proteins, and minerals.

Neuronal Pathways for Taste

Taste from the anterior two-thirds of the tongue, except from the circumvallate papillae, is carried by means of a branch of the facial nerve (VII) called the chorda tympani. Taste from the posterior one-third of the tongue, the circumvallate papillae, and the superior pharynx is carried by means of the glossopharyngeal nerve (IX). In addition to these two major nerves, the vagus nerve (X) carries a few .bers for taste sensation from the epiglottis. These nerves extend from the taste buds to the tractus solitarius of the medulla oblongata. Fibers from this nucleus decussate and extend to the thalamus. Neurons from the thalamus project to the taste area of the cortex, which is at the extreme inferior end of the postcentral gyrus.

Pathways for the Sense of Taste

The facial nerve (anterior two-thirds of the tongue), glossopharyngeal nerve (posterior one-third of the tongue), and vagus nerve (root of the tongue) all carry taste sensations. The trigeminal nerve is also shown. It carries tactile sensations from the anterior two-thirds of the tongue. The chorda tympani from the facial nerve (carrying taste input) joins the trigeminal nerve.

 

Smell

Olfaction (ol-fak_shu¢n), the sense of smell, occurs in response to odors that stimulate sensory receptors located in the extreme superior region of the nasal cavity, called the olfactory recess.

Most of the nasal cavity is involved in respiration, with only a small superior part devoted to olfaction. During normal respiration, air passes through the nasal cavity without much of it entering the olfactory recess. The major anatomic features of the nasal cavity are described in chapter 23 in relation to respiration. The specialized nasal epithelium of the olfactory recess is called the olfactory epithelium.

Like taste, smell is a chemical sense, but there are no basic sensations for smell, as there are for touch and taste. Unlike the retina’s receptor cells that sense color by breaking it into component parts, the 5 million olfactory receptor cells with their 1000 different receptor proteins recognize individual odor molecules. Some odors trigger a combination of receptors. Like other stimuli, odors can spontaneously evoke memories and feelings.

 

(a) The lateral wall of the nasal cavity (cut in sagittal section), showing the olfactory recess and olfactory bulb. (b) The olfactory cells within the olfactory epithelium are shown. The olfactory nerve processes passing through the cribriform plate and the .ne structure of the olfactory bulb are also shown.

 

The sensory stimuli that produce our sensation of an odor are molecules in the air. These airborne molecules are emitted by the substance we are smelling. We inhale them through the nose and through the opening in the palate at the back of the throat. In the nose, the molecules encounter millions of olfactory receptor cells located high in the nasal cavity. Unlike the sensory receptors for hearing and vision, the olfactory receptors are constantly being replaced. Each cell lasts for only about 30 to 60 days. In 1991, neuroscientists Linda Buck and Richard Axel identified the odor receptors that are present on the hairlike fibers of the olfactory neurons. Like synaptic receptors, each odor receptor seems to be specialized to respond to molecules of a different chemical structure. When these olfactory receptor cells are stimulated by the airborne molecules, the stimulation is converted into neural messages that pass along their axons, bundles of which make up the olfactory nerves.

So far, hundreds of different odor receptors have been identified (Mombaerts, 1999). We probably don’t have a separate receptor for each of the estimated 10,000 different odors that we can identify, however. Rather, each receptor is like a letter in an olfactory alphabet. Just as different combinations of letters in the alphabet are used to produce recognizable words, different combinations of olfactory receptors produce the sensation of distinct odors. Thus, the airborne molecules activate specific combinations of receptors, and the brain identifies an odor by interpreting the pattern of olfactory receptors that are stimulated (Buck, 2000).

The olfactory nerves directly connect to the olfactory bulb in the brain, which is actually the enlarged ending of the olfactory cortex at the front of the brain. Warren lost his sense of smell because the surgeon cut through the nerve fibers leading to his olfactory bulb. Axons from the olfactory bulb form the olfactory tract. These neural pathways project to different brain areas, including the temporal lobe and structures in the limbic system (Angier, 1995). The projections to the temporal lobe are thought to be part of the neural pathway involved in our conscious recognition of smells. The projections to the limbic system are thought to regulate our emotional response to odors. The direct connection of olfactory receptor cells to areas of the cortex and

limbic system is unique to our sense of smell. All other bodily sensations are first processed in the thalamus before being relayed to the higher brain centers in the cortex. Olfactory neurons are unique in another way, too. They are the only neurons that directly link the brain and the outside world (Axel, 1995). The axons of the sensory neurons that are located in your nose extend directly into your brain! As with the other senses, we experience sensory adaptation to odors when exposed to them for a period of time. In general, we reach maximum adaptation to an odor in less than a minute.We continue to smell the odor, but we have become about 70 percent less sensitive to it.

Olfactory Epithelium and Bulb

Ten million olfactory neurons are present within the olfactory epithelium. The axons of these bipolar neurons project through numerous small foramina of the bony cribriform plate to the olfactory bulbs. Olfactory tracts project from the bulbs to the cerebral cortex.

The dendrites of olfactory neurons extend to the epithelial surface of the nasal cavity, and their ends are modi.ed into bulbous enlargements called olfactory vesicles. These vesicles possess cilia called olfactory hairs, which lie in a thin mucous .lm on the epithelial surface. Airborne molecules enter the nasal cavity and are dissolved in the .uid covering the olfactory epithelium. Some of these molecules, referred to as odorants, bind to chemoreceptor molecules of the olfactory hair membranes. Although the exact nature of this interaction is not yet fully understood, it appears that the chemoreceptors are membrane receptor molecules that bind to odorants. Once an odorant has become bound to a receptor, the cilia of the olfactory neurons react by depolarizing and initiating action potentials in the olfactory neurons.

The mechanism of olfactory discrimination is not completely known. Most physiologists believe that the wide variety of detectable smells, which is about 4000 for the average person, are actually combinations of a smaller number of primary odors. Seven primary classes of odors have been proposed: (1) camphoraceous, (2)musky, (3) .oral, (4) pepperminty, (5) ethereal, (6) pungent, and (7) putrid. It’s very unlikely, however, that this list is an accurate representation of all primary odors, and some studies point to the possibility of as many as 50 primary odors.

The threshold for the detection of odors is very low, so very few odorant molecules are required to trigger the response. Apparently there is rather low speci.city in the olfactory epithelium. A given receptor may react to more than one type of odorant. The primary olfactory neurons have the most exposed nerve endings of any neurons, and they are constantly being replaced. The entire olfactory epithelium, including the neurosensory cells, is lost about every 2 months as the olfactory epithelium degenerates and is lost from the surface. Lost olfactory cells are replaced by a proliferation of basal cells in the olfactory epithelium. This replacement of olfactory neurons is unique among neurons, most of which are permanent cells that have a very limited ability to replicate.

Neuronal Pathways for Olfaction

Axons from the olfactory neurons (cranial nerve I) enter the olfactory bulb, where they synapse with mitral  cells or tufted cells. The mitral and tufted cells relay olfactory information to the brain through the olfactory tracts and synapse with association neurons in the olfactory bulb. Association neurons also receive input from nerve cell processes entering the olfactory bulb from the brain. As a result of input from both mitral cells and the brain, association neurons can modify olfactory information before it leaves the olfactory bulb. Olfaction is the only major sensation that is relayed directly to the cerebral cortex without first passing through the thalamus. Each olfactory tract terminates in an area of the brain called the olfactory cortex.

The olfactory cortex is in the frontal lobe, within the lateral .ssure of the cerebrum, and can be divided structurally and functionally into three areas: lateral, intermediate, and medial. The lateral olfactory area is involved in the conscious perception of smell. The medial olfactory area is responsible for visceral and emotional reactions to odors and has connections to the limbic system, through which it connects to the hypothalamus. Axons extend from the intermediate olfactory area along the olfactory tract to the bulb, synapse with the association neurons, and thus constitute a major mechanism by which sensory information is modulated within the olfactory bulb.

 

References:

1. Review of Medical Physiology // W.F.Ganong. – Twentieth edition, 2001. – P. 173 – 188/

2. Textbook of Medical Physiology // A.C.Guyton, J.E.Hall. – Tenth edition, 2002. – P. 602-611, 640-647.

3. Carlile S. and and King, A. J. (1993). From outer ear to virtual space. Current Biology, 3, 446–8.

4. Pickles, J. O. (1988). An introduction to the physiology of hearing, (2nd edn). Academic Press, London.