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
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.
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
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
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.