Download PHYSIOLOGICAL PSYCHOLOGY B.Sc. Counselling Psychology

PHYSIOLOGICAL
PSYCHOLOGY
III SEMESTER
Complementary Course
for
B.Sc. Counselling
Psychology
(CUCBCSS - 2014 Admission onwards)
UNIVERSITY OF CALICUT
SCHOOL OF DISTANCE EDUCATION
STUDY MATERIAL
Core Course
B.Sc. COUNSELLING PSYCHOLOGY
III Semester
UNIVERSITY OF CALICUT
physiological psychology
SCHOOL OF DISTANCE EDUCATION
Calicut university P.O, Malappuram Kerala, India 673 635.
School of Distance Education
UNIVERSITY OF CALICUT
SCHOOL OF DISTANCE EDUCATION
STUDY MATERIAL
PHYSIOLOGICAL PSYCHOLOGY
III Semester
Complementary Course
B.Sc. Counselling Psychology
Prepared by : Sri. Mohammed Junaid. A,
Research scholar,
Dept. of Psychology,
Calicut University.
Scrutinized by: Dr. Baby Shari P A,
Associate Professor,
Dept. of Psychology,
Calicut University.
Layout & Settings: Computer Section, SDE
© Reserved
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PAGES
CONTENT
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05-29
Module - II
30-40
Module -
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MODULE 1
SENSORY PROCESSES OTHER THAN VISION
THE SENSE OF HEARING
Structures of the outer, middle, and inner ear are involved in the sense of hearing. The
inner ear also contains structures that provide a sense of balance, or equilibrium. The
development of the ear begins during the fourth week and is complete by week 32. The
ear contains receptors that convert sound waves into nerve impulses and receptors that
respond to movements of the head. Impulses from both receptor types are transmitted
through the vestibule-cochlear nerve to the brain for interpretation.
Outer Ear
The outer ear consists of the auricle, or pinna, and the external acoustic canal. The
external acoustic canal is the fleshy tube that is fitted into the bony tube called the
external acoustic meatus. The auricle is the visible fleshy appendage attached to the
side of the head. It consists of a cartilaginous framework of elastic connective tissue
covered with skin. The rim of the auricle is the helix, and the inferior fleshy portion is
the earlobe. The earlobe is the only portion of the auricle that is not supported with
cartilage. The auricle has a ligamentous attachment to the skull and poorly developed
auricular muscles that insert within it anteriorly, superiorly, and posteriorly. The blood
supply to the auricle is from the posterior auricular and occipital arteries, which branch
from the external carotid and superficial temporal arteries, respectively. The structure
of the auricle directs sound waves into the external acoustic canal. The external
acoustic canal is a slightly S-shaped tube, about 2.5 cm long,that extends slightly
upward from the auricle to the tympanic membrane. The skin that lines the canal
contains fine hairs and sebaceous glands near the entrance. Deep within the canal, the
skin contains specialized wax secreting glands, called ceruminous glands. The cerumen
(earwax) secreted from these glands keeps the tympanic membrane soft and
waterproof. The cerumen and hairs also help to prevent small foreign objects from
reaching the tympanic membrane. The bitter cerumen is probably an insect repellent as
well. The tympanic membrane (“eardrum”) is a thin, double-layered, epithelial
partition, approximately 1 cm in diameter, between the external acoustic canal and the
middle ear. It is composed of an outer concave layer of stratified squamous epithelium
and an inner convex layer of low columnar epithelium.
Between the epithelial layers is a layer of connective tissue. The tympanic membrane is
extremely sensitive to pain and is innervated by the auriculotemporal nerve (a branch of
the mandibular nerve of the trigeminal nerve) and the auricular nerve (a branch of the
vagus nerve). Small sensory branches from the facial nerve and the glosopharyngeal
nerve also innervate the tympanic membrane.
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Middle Ear
The laterally compressed middle ear is an air-filled chamber called the tympanic cavity
in the petrous part of the temporal bone. The tympanic membrane separates the
middle ear from the external acoustic canal of the outer ear. A bony partition containing
the vestibular window (oval window) and the cochlear window (round window)
separates the middle ear from the inner ear. There are two openings into the tympanic
cavity. The epitympanic recess in the posterior wall connects the tympanic cavity to the
mastoidal air cells within the mastoid process of the temporal bone. The auditory
(eustachian) tube connects the tympanic cavity anteriorly with the nasopharynx and
equalizes air pressure on both sides of the tympanic membrane. Three auditory ossicles
extend across the tympanic cavity from the tympanic membrane to the vestibular
window. These tiny bones (the smallest in the body), from outer to inner, are the
malleus (hammer), incus (anvil), and stapes (stirrup). The auditory ossicles are attached
to the wall of the tympanic cavity by ligaments. Vibrations of the tympanic membrane
cause the auditory ossicles to move and transmit sound waves across the tympanic
cavity to the vestibular window. Vibration of the vestibular window moves a fluid within
the inner ear and stimulates the receptors of hearing.
As the auditory ossicles transmit vibrations from the tympanic membrane, they act as a
lever system to amplify sound waves. In addition, the sound waves are intensified as
they are transmitted from the relatively large surface of the tympanic membrane to the
smaller surface area of the vestibular window. The combined effect increases sound
amplification about 20 times.
Two small skeletal muscles, the tensor tympani muscle and the stapedius muscle,
attach to the malleus and stapes, respectively, and contract reflexively to protect the
inner ear against loud noises. When contracted, the tensor tympani muscle pulls the
malleus inward, and the stapedius muscle pulls the stapes outward. This combined
action reduces the force of vibration of the auditory ossicles.
Inner Ear
The entire structure of the inner ear is referred to as the labyrinth. The labyrinth
consists of an outer shell of dense bone called the bony labyrinth that surrounds and
protects a membranous labyrinth. The space between the bony labyrinth and the
membranous labyrinth is filled with a fluid called perilymph, which is secreted by cells
lining the bony canals. Within the tubular chambers of the membranous labyrinth is yet
another fluid called endolymph. These two fluids provide a liquid-conducting medium
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for the vibrations involved in hearing and the maintenance of equilibrium. The bony
labyrinth is structurally and functionally divided into three areas: the vestibule,
semicircular canals, and cochlea. The functional organs for hearing and equilibrium are
located in these areas.
Vestibule
The vestibule is the central portion of the bony labyrinth. It contains the vestibular
(oval) window, into which the stapes fits, and the cochlear (round) window on the
opposite end.
The membranous labyrinth within the vestibule consists of two connected sacs called
the utricle and the saccule. The utricle is larger than the saccule and lies in the upper
back portion of the vestibule. Both the utricle and saccule contain receptors that are
sensitive to gravity and linear movement (acceleration) of the head.
Semicircular Canals
Posterior to the vestibule are the three bony semicircular canals, positioned at nearly
right angles to each other. The thinner semicircular ducts form the membranous
labyrinth within the semicircular canals. Each of the three semicircular ducts has a
membranous ampulla at one end and connects with the upper back part of the utricle.
Receptors within the semicircular ducts are sensitive to angular acceleration and
deceleration of the head, as in rotational movement.
Cochlea
The snail-shaped cochlea is coiled two and a half times around a central core of bone.
There are three chambers in the cochlea. The upper chamber, the scala vestibuli, begins
at the vestibular window and extends to the apex (end) of the coiled cochlea. The lower
chamber, the scala tympani, begins at the apex and terminates at the cochlear window.
Both the scala vestibuli and the scala tympani are filled with perilymph. They are
completely separated, except at the narrow apex of the cochlea, called the helicotrema
where they are continuous. Between the scala vestibuli and the scala tympani is the
cochlear duct, the triangular middle chamber of the cochlea. The roof of the cochlear
duct is called the vestibular membrane, and the floor is called the basilar membrane.
The cochlear duct, which is filled with endolymph, ends at the helicotrema.
Within the cochlear duct is a specialized structure called the spiral organ (organ of
Corti). The sound receptors that transform mechanical vibrations into nerve impulses
are located along the basilar membrane of this structure, making it the functional unit of
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hearing. The epithelium of the spiral organ consists of supporting cells and hair cells.
The bases of the hair cells are anchored in the basilar membrane, and their tips are
embedded in the tectorial membrane, which forms a gelatinous canopy over them.
Sound Waves and Neural Pathways for Hearing
Sound Waves
Sound waves travel in all directions from their source, like ripples in a pond after a stone
is dropped. These waves of energy are characterized by their frequency and their
intensity. The frequency, or number of waves that pass a given point in a given time, is
measured in hertz (Hz). The pitch of a sound is directly related to its frequency—the
higher the frequency of a sound, the higher its pitch. For example, striking the high C on
a piano produces a high frequency of sound that has a high pitch. The intensity, or
loudness of a sound, is directly related to the amplitude of the sound waves. Sound
intensity is measured in units known as decibels (dB). A sound that is barely audible—at
the threshold of hearing—has an intensity of zero decibels. Every 10 decibels indicates a
tenfold increase in sound intensity: a sound is 10 times higher than threshold at 10 dB,
100 times higher at 20 dB, a million times higher at 60 dB, and 10 billion times higher at
100 dB. The healthy human ear can detect very small differences in sound intensity—
from 0.1 to 0.5 dB. Sound waves funneled through the external acoustic canal produce
extremely small vibrations of the tympanic membrane. Movements of the tympanum
during ordinary speech (with an average intensity of 60 dB) are estimated to be equal to
the diameter of a molecule of hydrogen. Sound waves passing through the solid
medium of the auditory ossicles are amplified about 20 times as they reach the
footplate of the stapes, which is seated within the vestibular window.
As the vestibular window is displaced, pressure waves pass through the fluid medium of
the scala vestibuli and pass around the helicotrema to the scala tympani. Movements of
perilymph within the scala tympani, in turn, displace the cochlear window into the
tympanic cavity.
When the sound frequency (pitch) is sufficiently low, there is adequate time for the
pressure waves of perilymph within the scala vestibuli to travel around the helicotrema
to the scala tympani. As the sound frequency increases, however, these pressure waves
do not have time to travel all the way to the apex of the cochlea. Instead, they are
transmitted through the vestibular membrane, which separates the scala vestibuli from
the cochlear duct, and through the basilar membrane, which separates the cochlear
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duct from the scala tympani, to the perilymph of the scala tympani. The distance that
these pressure waves travel, therefore, decreases as the sound frequency increases.
Neural Pathways for Hearing
Cochlear sensory neurons in the vestibulocochlear nerve synapse with neurons in the
medulla oblongata, which project to the inferior colliculi of the midbrain. Neurons in this
area in turn project to the thalamus, which sends axons to the auditory cortex of the
temporal lobe, where the auditory sensations (nerve impulses) are perceived as sound.
AUDITORY LOCALIZATION
The process of recognizing where a sound is coming from is analogous to recognizing
depth or distance in vision. Both processes involve spatial aspects of sensory input.
Many features contribute to auditory localization of which the following are most
important:
Having two ears
In the same way that having two eyes allows for greater visual abilities through
stereoscopic vision, so having two ears affords a greater skill in hearing. The use of two
ears is called binaural detection. Without two ears, our ability to locate a sound source
is diminished, although, as we shall see, not completely eradicated.
Phase difference and sonic shadow
When sound comes from one side or the other, two cues are available to help locate its
source. The first cue comes from the fact that the sound will reach one ear prior to the
other. This creates an arrival time difference (also known as a latency difference),
which can be detected by neurons in the superior olive. Cells here are tuned to
particular arrival time differences and can detect differences in arrival time at the two
ears that are as small as a fraction of a millisecond. Differences in arrival time are
adequate to locate a sound source if the sound is a simple and discrete one (for
example, a click), but a variation of this is needed to explain our ability to locate more
complex or continuous sounds.
Phase difference
Phase difference refers to the fact that different portions (phases) of the sound wave
arrive at each ear at any one time. That is, while one ear is stimulated by a high pressure
part of the sound wave, the other might be stimulated by a lower pressure part. These
phase differences have the following consequence. Sound waves cause the eardrum to
be pushed in and pulled out (i.e. to vibrate). Phase differences will mean that whilst,
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say, the right eardrum is pushed in, the left eardrum might simultaneously be pulled
out. If the eardrum positions were exactly opposite, then the phase difference would be
180˚. Given that the phase difference for sounds directly in the midline will be zero and
the maximal phase difference is 180˚, the combination of phase difference and sound
frequency will give an indication of the sound’s location. This information is more useful
for low frequency sounds than for high frequency sounds because of the wavelength
and the distance separating the ears. Neurons of the medial superior olive are able to
use this phase difference as an aid to locating the source of the sound.
A second cue to location comes from sound intensity differences that arise from what is
called the sonic shadow. This method of detection is particularly useful for high
frequency sounds when the phase differences become too small to detect as the
wavelengths of the sound become shorter. Information that comes from one side of the
head will be more intense in the nearer ear and less intense in the further ear. The head
is in the way of the further ear and absorbs high frequency sounds. Cells in the lateral
superior olive and the auditory cortex can detect these intensity differences.
These two mechanisms are complementary, providing a comprehensive system for the
localization of sounds. Low frequency sounds produce phase differences but do not
produce great differences in intensity at the two ears. Higher-frequency sounds produce
poor phase differences but create a strong sonic shadow. The combination of both
mechanisms allows for the detection of the location of sound across the whole
frequency range and is known as the duplex theory.
Monaural cues
People who are deaf in one ear are not completely unable to localize sound. Monaural
cues to the location of sound come from the pinnae of the outer ear.
The pinnae dampen and filter the sound that enters the ear canal (known as spectral
filtering). The modulations that occur will depend in part on the direction that the
sound is coming from. Our ability to detect these differences gives us a localization cue.
We need to appreciate here that our ability to recognize these changes alters as our
head and ears grow from childhood into adulthood.
Differentiating ‘in front’ from ‘behind
Two sounds that are located an equal distance from your ears in the midline, where one
is in front and one is behind, will be difficult to distinguish. There will be no difference of
phase or latency, and the intensities of the sounds at the two ears will be identical. The
knowledge of whether the sound is coming from in front or from behind relies on the
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pinnae of the outer ear. The differences in reflection of sound by the folds of the pinnae
will differ for the two sound sources. Interestingly, sound location is best in the
horizontal plane and much poorer for the near–far, in front–behind, and up–down
directions.
THEORIES OF HEARING
Theories of hearing account for how sound waves are physiologically translated into the
perceptions of pitch, loudness, and timbre. To date, most of the theorizing about
hearing has focused on the perception of pitch, which is reasonably well understood.
Researchers’ understanding of loudness and timbre perception is primitive by
comparison. Hence, we’ll limit our coverage to theories of pitch perception.
Two theories have dominated the debate on pitch perception: place theory and
frequency theory. For better understatnding of these theories, imagine the spiraled
cochlea unraveled, so that the basilar membrane becomes a long, thin sheet, lined with
about 25,000 individual hair cells.
Place Theory
Long ago, Hermann von Helmholtz (1863) proposed that specific sound frequencies
vibrate specific portions of the basilar membrane, producing distinct pitches, just as
plucking specific strings on a harp produces sounds of varied pitch. This model, called
place theory, holds that perception of pitch corresponds to the vibration of different
portions, or places, along the basilar membrane. Place theory assumes that hair cells at
various locations respond independently and that different sets of hair cells are vibrated
by different sound frequencies. The brain then detects the frequency of a tone
according to which area along the basilar membrane is most active.
Evidence that this place coding theory is correct comes from two sources. High doses of
antibiotics, such as kanamycin, can cause damage to the basilar membrane by inducing
hair cell loss. This loss starts at the base of the membrane and higher frequencies are
affected first (Stebbins et al., 1969). The other source of evidence is the success of
cochlear implants. If a person is deaf because of the loss of basilar membrane
stimulation, a cochlear implant device can be implanted that mechanically converts the
sound waves into vibrations at different regions of the membrane according to the
frequency. Provided that the basilar membrane and all later aspects of the auditory
system are functioning normally, hearing will be restored.
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Frequency Theory
Other theorists in the 19th century proposed an alternative theory of pitch perception,
called frequency theory (Rutherford, 1886). Frequency theory holds that perception of
pitch corresponds to the rate, or frequency, at which the entire basilar membrane
vibrates. This theory views the basilar membrane as more like a drumhead than a harp.
According to frequency theory, the whole membrane vibrates in unison in response to
sounds. However, a particular sound frequency, say 3000 Hz, causes the basilar
membrane to vibrate at a corresponding rate of 3000 times per second. The brain
detects the frequency of a tone by the rate at which the auditory nerve fibers fire.
The Two Theories of Hearing Combined
Although the original theories had to be revised, the current thinking is that pitch
perception depends on both place and frequency coding of vibrations along the basilar
membrane (Goldstein, 1996). Sounds under 1000 Hz appear to be translated into pitch
through frequency coding. For sounds between 1000 and 5000 Hz, pitch perception
seems to depend on a combination of frequency and place coding. Sounds over 5000 Hz
seem to be handled through place coding only. Again we find that theories that were
pitted against each other for decades are complementary rather than contradictory.
For additional reading:
The volley principle (Wever and Bray, 1937)
The volley principle holds that groups of auditory nerve fibers fire neural impulses in
rapid succession, creating volleys of impulses. These volleys exceed the 1000 per-second
limit.
SENSATIONS OF TASTE AND SMELL
The senses of taste and smell allow us to separate undesirable or even lethal foods from
those that are pleasant to eat and nutritious. The sense of smell also allows animals to
recognize the proximity of other animals or even individuals among animals. Finally,
both senses are strongly tied to primitive emotional and behavioral functions of our
nervous systems.
Primary Sensations of Taste
The identities of the specific chemicals that excite different taste receptors are not all
known. Even so, psychophysiologic and neurophysiologic studies have identified at least
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13 possible or probable chemical receptors in the taste cells.
For practical analysis of taste, the aforementioned receptor capabilities have also been
grouped into five general categories called the primary sensations of taste. They are
sour, salty, sweet, bitter, and "umami."
A person can perceive hundreds of different tastes. They are all supposed to be
combinations of the elementary taste sensations, just as all the colors we can see are
combinations of the three primary colors.
Sour Taste. The sour taste is caused by acids, that is, by the hydrogen ion concentration,
and the intensity of this taste sensation is approximately proportional to the logarithm
of the hydrogen ion concentration. That is, the more acidic the food, the stronger the
sour sensation becomes.
Salty Taste. The salty taste is elicited by ionized salts, mainly by the sodium ion
concentration. The quality of the taste varies somewhat from one salt to another,
because some salts elicit other taste sensations in addition to saltiness.
Sweet Taste. The sweet taste is not caused by any single class of chemicals. Some of the
types of chemicals that cause this taste include sugars, glycols, alcohols, aldehydes,
ketones, amides, esters, some amino acids , some small proteins, sulfonic acids,
halogenated acids, and inorganic salts of lead and beryllium. Note specifically that most
of the substances that cause a sweet taste are organic chemicals. It is especially
interesting that slight changes in the chemical structure, such as addition of a simple
radical, can often change the substance from sweet to bitter.
Bitter Taste. The bitter taste, like the sweet taste, is not caused by any single type of
chemical agent. Here again, the substances that give the bitter taste are almost entirely
organic substances. Two particular classes of substances are especially likely to cause
bitter taste sensations: (1) long-chain organic substances that contain nitrogen, and (2)
alkaloids.
Some substances that at first taste sweet have a bitter aftertaste. This is true of
saccharin, which makes this substance objectionable to some people.
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The bitter taste, when it occurs in high intensity, usually causes the person or animal to
reject the food. This is undoubtedly an important function of the bitter taste sensation,
because many deadly toxins found in poisonous plants are alkaloids, and virtually all of
these cause intensely bitter taste, usually followed by rejection of the food.
Umami Taste. Umami is a Japanese word (meaning "delicious") designating a pleasant
taste sensation that is qualitatively different from sour, salty, sweet, or bitter. Umami is
the dominant taste of food containing L-glutamate, such as meat extracts and aging
cheese, and some physiologists consider it to be a separate, fifth category of primary
taste stimuli.
Taste Blindness. Some people are taste blind for certain substances, especially for
different types of thiourea compounds. A substance used frequently by psychologists
for demonstrating taste blindness is phenylthiocarbamide, for which about 15 to 30 per
cent of all people exhibit taste blindness; the exact percentage depends on the method
of testing and the concentration of the substance.
Taste Bud and Its Function
A taste bud has a diameter of about 1/30 millimeter and a length of about 1/16
millimeter. The taste bud is composed of about 50 modified epithelial cells, some of
which are supporting cells called sustentacular cells and others of which are taste cells.
The taste cells are continually being replaced by mitotic division of surrounding
epithelial cells, so that some taste cells are young cells. Others are mature cells that lie
toward the center of the bud; these soon break up and dissolve. The life span of each
taste cell is about 10 days in lower mammals but is unknown for humans.
The outer tips of the taste cells are arranged around a minute taste pore. From the tip of
each taste cell, several microvilli, or taste hairs, protrude outward into the taste pore to
approach the cavity of the mouth. These microvilli provide the receptor surface for
taste.
Interwoven around the bodies of the taste cells is a branching terminal network of taste
nerve fibers that are stimulated by the taste receptor cells. Some of these fibers
invaginate into folds of the taste cell membranes. Many vesicles form beneath the cell
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membrane near the fibers. It is believed that these vesicles contain a neurotransmitter
substance that is released through the cell membrane to excite the nerve fiber endings
in response to taste stimulation.
Location of the Taste Buds. The taste buds are found on three types of papillae of the
tongue, as follows:
(1) A large number of taste buds are on the walls of the troughs that surround the
circumvallate papillae, which form a V line on the surface of the posterior tongue.
(2) Moderate numbers of taste buds are on the fungiform papillae over the flat anterior
surface of the tongue.
(3) Moderate numbers are on the foliate papillae located in the folds along the lateral
surfaces of the tongue.
Additional taste buds are located on the palate, and a few are found on the tonsillar
pillars, on the epiglottis, and even in the proximal esophagus. Adults have 3000 to
10,000 taste buds, and children have a few more. Beyond the age of 45 years, many
taste buds degenerate, causing the taste sensation to become progressively less critical
in old age.
Specificity of Taste Buds for a Primary Taste Stimulus. Microelectrode studies from
single taste buds show that each taste bud usually responds mostly to one of the five
primary taste stimuli when the taste substance is in low concentration. But at high
concentration, most buds can be excited by two or more of the primary taste stimuli, as
well as by a few other taste stimuli that do not fit into the "primary" categories.
Mechanism of Stimulation of Taste Buds
Receptor Potential. The membrane of the taste cell, like that of most other sensory
receptor cells, is negatively charged on the inside with respect to the outside.
Application of a taste substance to the taste hairs causes partial loss of this negative
potential-that is, the taste cell becomes depolarized. In most instances, the decrease in
potential, within a wide range, is approximately proportional to the logarithm of
concentration of the stimulating substance. This change in electrical potential in the
taste cell is called the receptor potential for taste.
The mechanism by which most stimulating substances react with the taste villi to initiate
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the receptor potential is by binding of the taste chemical to a protein receptor molecule
that lies on the outer surface of the taste receptor cell near to or protruding through a
villus membrane. This, in turn, opens ion channels, which allows positively charged
sodium ions or hydrogen ions to enter and depolarize the normal negativity of the cell.
Then the taste chemical itself is gradually washed away from the taste villus by the
saliva, which removes the stimulus.
The type of receptor protein in each taste villus determines the type of taste that will be
perceived. For sodium ions and hydrogen ions, which elicit salty and sour taste
sensations, respectively, the receptor proteins open specific ion channels in the apical
membranes of the taste cells, thereby activating the receptors. However, for the sweet
and bitter taste sensations, the portions of the receptor protein molecules that protrude
through the apical membranes activate second-messenger transmitter substances inside
the taste cells, and these second messengers cause intracellular chemical changes that
elicit the taste signals.
Adaptation of Taste
Everyone is familiar with the fact that taste sensations adapt rapidly, often almost
completely within a minute or so of continuous stimulation. Yet, from
electrophysiological studies of taste nerve fibers, it is clear that adaptation of the taste
buds themselves usually accounts for no more than about half of this. Therefore, the
final extreme degree of adaptation that occurs in the sensation of taste almost certainly
occurs in the central nervous system itself, although the mechanism and site of this are
not known. At any rate, it is a mechanism different from that of most other sensory
systems, which adapt almost entirely at the receptors.
The phenomenon of taste preference almost certainly results from some mechanism
located in the central nervous system and not from a mechanism in the taste receptors
themselves, although it is true that the receptors often become sensitized in favor of a
needed nutrient.
Gustatory information is conveyed along cranial nerves to the nucleus of the solitary
tract in the medulla. From there, neurons travel to the thalamus, and from there to the
primary sensory region of the cerebral cortex, the amygdale and the hypothalamus.
Smell
Smell is the least understood of our senses. This results partly from the fact that the
sense of smell is a subjective phenomenon that cannot be studied with ease in lower
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animals. Another complicating problem is that the sense of smell is poorly developed in
human beings in comparison with the sense of smell in many lower animals.
Olfactory Membrane
The olfactory membrane lies in the superior part of each nostril. Medially, the olfactory
membrane folds downward along the surface of the superior septum; laterally, it folds
over the superior turbinate and even over a small portion of the upper surface of the
middle turbinate. In each nostril, the olfactory membrane has a surface area of about
2.4 square centimeters.
Olfactory Cells. The receptor cells for the smell sensation are the olfactory cells, which
are actually bipolar nerve cells derived originally from the central nervous system itself.
There are about 100 million of these cells in the olfactory epithelium interspersed
among sustentacular cells. The mucosal end of the olfactory cell forms a knob from
which 4 to 25 olfactory hairs (also called olfactory cilia), measuring 0.3 micrometer in
diameter and up to 200 micrometers in length, project into the mucus that coats the
inner surface of the nasal cavity. These projecting olfactory cilia form a dense mat in the
mucus, and it is these cilia that react to odors in the air and stimulate the olfactory cells.
Spaced among the olfactory cells in the olfactory membrane are many small Bowman's
glands that secrete mucus onto the surface of the olfactory membrane.
Stimulation of the Olfactory Cells
Mechanism of Excitation of the Olfactory Cells. The portion of each olfactory cell that
responds to the olfactory chemical stimuli is the olfactory cilia. The odorant substance,
on coming in contact with the olfactory membrane surface, first diffuses into the mucus
that covers the cilia. Then it binds with receptor proteins in the membrane of each
cilium. Each receptor protein is actually a long molecule that threads its way through the
membrane about seven times, folding inward and outward. The odorant binds with the
portion of the receptor protein that folds to the outside. The inside of the folding
protein, however, is coupled to a so-called G-protein, itself a combination of three
subunits. On excitation of the receptor protein, an alpha subunit breaks away from the
G-protein and immediately activates adenylyl cyclase, which is attached to the inside of
the ciliary membrane near the receptor cell body. The activated cyclase, in turn,
converts many molecules of intracellular adenosine triphosphate into cyclic adenosine
monophosphate (cAMP). Finally, this cAMP activates another nearby membrane protein,
a gated sodium ion channel, that opens its "gate" and allows large numbers of sodium
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ions to pour through the membrane into the receptor cell cytoplasm. The sodium ions
increase the electrical potential in the positive direction inside the cell membrane, thus
exciting the olfactory neuron and transmitting action potentials into the central nervous
system by way of the olfactory nerve.
The importance of this mechanism for activating olfactory nerves is that it greatly
multiplies the excitatory effect of even the weakest odorant. To summarize, the process
works as follows:
(1) Activation of the receptor protein by the odorant substance activates the G-protein
complex.
(2) This, in turn, activates multiple molecules of adenylyl cyclase inside the olfactory cell
membrane.
(3) This causes the formation of many times more molecules of cAMP.
(4) Finally, the cAMP opens still many times more sodium ion channels. Therefore, even
the most minute concentration of a specific odorant initiates a cascading effect that
opens extremely large numbers of sodium channels. This accounts for the exquisite
sensitivity of the olfactory neurons to even the slightest amount of odorant.
In addition to the basic chemical mechanism by which the olfactory cells are stimulated,
several physical factors affect the degree of stimulation. First, only volatile substances
that can be sniffed into the nostrils can be smelled. Second, the stimulating substance
must be at least slightly water soluble so that it can pass through the mucus to reach the
olfactory cilia. Third, it is helpful for the substance to be at least slightly lipid soluble,
presumably because lipid constituents of the cilium itself are a weak barrier to non-lipidsoluble odorants.
Transmission of Smell Signals into the Central Nervous System
The olfactory portions of the brain were among the first brain structures developed in
primitive animals, and much of the remainder of the brain developed around these
olfactory beginnings. In fact, part of the brain that originally subserved olfaction later
evolved into the basal brain structures that control emotions and other aspects of
human behavior; this is the system we call the limbic system.
Transmission of Olfactory Signals into the Olfactory Bulb.
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The olfactory nerve fibers leading backward from the bulb are called cranial nerve I, or
the olfactory tract. However, in reality, both the tract and the bulb are an anterior
outgrowth of brain tissue from the base of the brain; the bulbous enlargement at its
end, the olfactory bulb, lies over the cribriform plate, separating the brain cavity from
the upper reaches of the nasal cavity. The cribriform plate has multiple small
perforations through which an equal number of small nerves pass upward from the
olfactory membrane in the nasal cavity to enter the olfactory bulb in the cranial cavity.
Each bulb has several thousand glomeruli- short axons from the olfactory cells
terminating in multiple globular structures within the olfactory bulb- each of which is
the terminus for about 25,000 axons from olfactory cells. Each glomerulus also is the
terminus for dendrites from about 25 large mitral cells and about 60 smaller tufted cells,
the cell bodies of which lie in the olfactory bulb superior to the glomeruli. These
dendrites receive synapses from the olfactory cell neurons, and the mitral and tufted
cells send axons through the olfactory tract to transmit olfactory signals to higher levels
in the central nervous system.
 Only about 2% of inhaled air comes in contact with the olfactory receptors, which
are positioned in the nasal mucosa above the mainstream of airflow. Olfactory
sensitivity can be increased by forceful sniffing, which draws the air into contact
with the receptors.
PAIN
The receptors for pain are free nerve endings distributed throughout the skin as well as
in muscles, joints and internal organs. These are called nociceptors. They respond to
stimulation that damages tissues, including mechanical injury (e.g. cutting, crushing),
chemical damage (e.g. corrosive substances) and extremes of temperature (burning or
freezing). Within the tissues, the nerve endings are stimulated by various chemicals
produced by or released from damaged tissues. These include potassium ions from
damaged cells, bradykinin from blood plasma leaking from damaged blood vessels, and
histamine from mast cells, which form part of the mechanism of inflammation.
Damaged cells also produce prostaglandins, which seem to sensitize nerve endings to
other substances. The analgesic (pain-relieving) drug aspirin acts by preventing the
synthesis of prostaglandins.
Many, if not most, ailments of the body cause pain. Furthermore, the ability to diagnose
different diseases depends to a great extent on a physician's knowledge of the different
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qualities of pain.
Pain Is a Protective Mechanism
Pain occurs whenever any tissues are being damaged, and it causes the individual to
react to remove the pain stimulus. Even such simple activities as sitting for a long time
can cause tissue destruction because of lack of blood flow to the skin where it is
compressed by the weight of the body. When the skin becomes painful as a result of the
ischemia, the person normally shifts weight subconsciously. But a person who has lost
the pain sense, as after spinal cord injury, fails to feel the pain and, therefore, fails to
shift. This soon results in total breakdown and desquamation of the skin at the areas of
pressure.
Types of Pain and Their Qualities-Fast Pain and Slow Pain
Pain has been classified into two major types: fast pain and slow pain. Fast pain is felt
within about 0.1 second after a pain stimulus is applied, whereas slow pain begins only
after 1 second or more and then increases slowly over many seconds and sometimes
even minutes. The conduction pathways for these two types of pain are different and
each of them has specific qualities.
Fast pain is also described by many alternative names, such as sharp pain, pricking pain,
acute pain, and electric pain. This type of pain is felt when a needle is stuck into the skin,
when the skin is cut with a knife, or when the skin is acutely burned. It is also felt when
the skin is subjected to electric shock. Fast-sharp pain is not felt in deeper tissues of the
body.
Slow pain also goes by many names, such as slow burning pain, aching pain, throbbing
pain, nauseous pain, and chronic pain. This type of pain is usually associated with tissue
destruction. It can lead to prolonged, unbearable suffering. It can occur both in the skin
and in almost any deep tissue or organ.
Pain Receptors and Their Stimulation
Pain Receptors Are Free Nerve Endings
The pain receptors in the skin and other tissues are all free nerve endings. They are
widespread in the superficial layers of the skin as well as in certain internal tissues, such
as the periosteum, the arterial walls, the joint surfaces, and the falx and tentorium in the
cranial vault. Most other deep tissues are only sparsely supplied with pain endings;
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nevertheless, any widespread tissue damage can summate to cause the slow-chronicaching type of pain in most of these areas.
Three Types of Stimuli Excite Pain Receptors-Mechanical, Thermal, and Chemical
Pain can be elicited by multiple types of stimuli. They are classified as mechanical,
thermal, and chemical pain stimuli. In general, fast pain is elicited by the mechanical and
thermal types of stimuli, whereas slow pain can be elicited by all three types.
Some of the chemicals that excite the chemical type of pain are bradykinin, serotonin,
histamine, potassium ions, acids, acetylcholine, and proteolytic enzymes. In addition,
prostaglandins and substance P enhance the sensitivity of pain endings but do not
directly excite them. The chemical substances are especially important in stimulating the
slow, suffering type of pain that occurs after tissue injury.
Non-adapting Nature of Pain Receptors
In contrast to most other sensory receptors of the body, pain receptors adapt very little
and sometimes not at all. In fact, under some conditions, excitation of pain fibers
becomes progressively greater, especially so for slow-aching-nauseous pain, as the pain
stimulus continues. This increase in sensitivity of the pain receptors is called
hyperalgesia. One can readily understand the importance of this failure of pain
receptors to adapt, because it allows the pain to keep the person apprised of a tissue
damaging stimulus as long as it persists.
Rate of Tissue Damage as a Stimulus for Pain
The average person begins to perceive pain when the skin is heated above 45°C. This is
also the temperature at which the tissues begin to be damaged by heat; indeed, the
tissues are eventually destroyed if the temperature remains above this level indefinitely.
Therefore, it is immediately apparent that pain resulting from heat is closely correlated
with the rate at which damage to the tissues is occurring and not with the total damage
that has already occurred.
The intensity of pain is also closely correlated with the rate of tissue damage from
causes other than heat, such as bacterial infection, tissue ischemia, tissue contusion,
and so forth.
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Tissue Ischemia as a Cause of Pain
When blood flow to a tissue is blocked, the tissue often becomes very painful within a
few minutes. The greater the rate of metabolism of the tissue, the more rapidly the pain
appears. For instance, if a blood pressure cuff is placed around the upper arm and
inflated until the arterial blood flow ceases, exercise of the forearm muscles sometimes
can cause muscle pain within 15 to 20 seconds. In the absence of muscle exercise, the
pain may not appear for 3 to 4 minutes even though the muscle blood flow remains
zero.
Muscle Spasm as a Cause of Pain
Muscle spasm is also a common cause of pain, and it is the basis of many clinical pain
syndromes. This pain probably results partially from the direct effect of muscle spasm in
stimulating mechano-sensitive pain receptors, but it might also result from the indirect
effect of muscle spasm to compress the blood vessels and cause ischemia. Also, the
spasm increases the rate of metabolism in the muscle tissue, thus making the relative
ischemia even greater, creating ideal conditions for the release of chemical paininducing substances.
Dual Pathways for Transmission of Pain Signals into the Central Nervous System
Even though all pain receptors are free nerve endings, these endings use two separate
pathways for transmitting pain signals into the central nervous system. The two
pathways mainly correspond to the two types of pain-a fast-sharp pain pathway and a
slow-chronic pain pathway.
Peripheral Pain Fibers-"Fast" and "Slow" Fibers
The fast-sharp pain signals are elicited by either mechanical or thermal pain stimuli; they
are transmitted in the peripheral nerves to the spinal cord by small type Aδ fibers at
velocities between 6 and 30 m/sec. Conversely, the slow-chronic type of pain is elicited
mostly by chemical types of pain stimuli but sometimes by persisting mechanical or
thermal stimuli. This slow-chronic pain is transmitted to the spinal cord by type C fibers
at velocities between 0.5 and 2 m/sec.
Because of this double system of pain innervation, a sudden painful stimulus often gives
a "double" pain sensation: a fast-sharp pain that is transmitted to the brain by the Aδ
fiber pathway, followed a second or so later by a slow pain that is transmitted by the C
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fiber pathway. The sharp pain apprises the person rapidly of a damaging influence and,
therefore, plays an important role in making the person react immediately to remove
himself or herself from the stimulus. The slow pain tends to become greater over time.
This sensation eventually produces the intolerable suffering of long-continued pain and
makes the person keep trying to relieve the cause of the pain.
On entering the spinal cord from the dorsal spinal roots, the pain fibers terminate on
relay neurons in the dorsal horns. Here again, there are two systems for processing the
pain signals on their way to the brain.
While pain information is clearly represented in the cortex (otherwise we would not be
aware of it), it is not localized in the same way as tactile information. Pain information is
known to be passed from the thalamus to the cingulated cortex, which is part of the
limbic system. Limbic system is involved in emotional experience and behavior. Pain is
usually described as having affective (emotional) as well as sensory components.
Emotional and ‘higher-level’ cognitive processes can control the experience of pain. For
example, if a person in acute pain is given an injection of pure water, believing it to be
morphine, their pain will be dramatically relieved. This is an example of a placebo effect.
Similarly, pain can be made worse by fear, for example if the sufferer believes it to result
from a life-threatening illness rather than a trivial disorder.
Melzack and Wall (1965) proposed a gate-control theory to explain such top-down
effects on pain perception. The core of the theory is that stimulation of A fibers inhibits
the firing of C fibers, thereby effectively closing a ‘gate’ for pain signals. This stimulation
can come from cutaneous sensations, and is the basis for pain reduction when nearby
areas of skin are strongly stimulated, for example by vigorous rubbing. The stimulation
of the A fibers can also come from descending neurons from the brain, which is the
route for the top-down influences of pain. One such pathway originates in the
periaqueductal gray (PAG) region of the midbrain. Stimulation of the PAG reduces pain
sensation. Analgesic drugs such as morphine act on receptors in the PAG. It is supposed
that endorphins, which are produced by the body, reduce pain by acting on these
receptors.
Pain Suppression ("Analgesia") System in the Brain and Spinal Cord
The degree to which a person reacts to pain varies tremendously. This results partly
from a capability of the brain itself to suppress input of pain signals to the nervous
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system by activating a pain control system, called an analgesia system.
The analgesia system consists of three major components: (1) The periaqueductal gray
and periventricular areas of the mesencephalon and upper pons surround the aqueduct
of Sylvius and portions of the third and fourth ventricles. Neurons from these areas send
signals to (2) the raphe magnus nucleus, a thin midline nucleus located in the lower
pons and upper medulla, and the nucleus reticularis paragigantocellularis, located
laterally in the medulla. From these nuclei, second-order signals are transmitted down
the dorsolateral columns in the spinal cord to (3) a pain inhibitory complex located in the
dorsal horns of the spinal cord. At this point, the analgesia signals can block the pain
before it is relayed to the brain.
Electrical stimulation either in the periaqueductal gray area or in the raphe magnus
nucleus can suppress many strong pain signals entering by way of the dorsal spinal
roots. Also, stimulation of areas at still higher levels of the brain that excite the
periaqueductal gray area can also suppress pain. Some of these areas are (1) the
periventricular nuclei in the hypothalamus, lying adjacent to the third ventricle, and (2)
to a lesser extent, the medial forebrain bundle, also in the hypothalamus.
For additional reading:
Referred Pain
Through precise neural pathways, the brain is able to perceive the area of stimulation
and project the pain sensation back to that area. The sensation of pain from certain
visceral organs, however, may not be perceived as arising from those organs but from
other somatic locations. This phenomenon is known as referred pain. The sensation of
referred pain is relatively consistent from one person to another and is clinically
important in diagnosing organ dysfunctions. The pain of a heart attack, for example,
may be perceived subcutaneously over the heart and down the medial side of the left
arm. Ulcers of the stomach may cause pain that is perceived as coming from the upper
central (epigastric) region of the trunk.
Phantom Pain
Phantom pain is frequently experienced by an amputee who continues to feel pain from
the body part that was amputated, as if it were still there. After amputation, the
severed sensory neurons heal and function in the remaining portion of the appendage.
Although it is not known why impulses that are interpreted as pain are sent periodically
through these neurons, the sensations evoked in the brain are projected to the region of
the amputation, resulting in phantom pain.
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TACTILE AND PRESSURE RECEPTORS
Both tactile receptors and pressure receptors are sensitive to mechanical forces that
distort or displace the tissue in which they are located. Tactile receptors respond to
fine, or light, touch and are located primarily in the dermis and hypodermis of the skin.
Pressure receptors respond to pressure, vibration, and stretch and are commonly found
in the hypodermis of the skin and in the tendons and ligaments of joints.
Corpuscles of Touch
A corpuscle of touch (Meissner’s corpuscle) is an oval receptor composed of a mass of
dendritic endings from two or three nerve fibers enclosed by connective tissue sheaths.
These corpuscles are numerous in the hairless portions of the body, such as the eyelids,
lips, tip of the tongue, fingertips, palms of the hands, soles of the feet, nipples, and
external genitalia. Corpuscles of touch lie within the papillary layer of the dermis, where
they are especially sensitive to the movement of objects that barely contact the skin.
Free Nerve Endings
Free nerve endings are the least modified and the most superficial of the tactile
receptors. These receptors extend into the lower layers of the epidermis, where they
end as knobs between the epithelial cells. Free nerve endings respond chiefly to pain
and temperature, but they also detect touch and pressure, for example from clothing.
Some free nerve endings are particularly sensitive to tickle and itch.
Root Hair Plexuses
Root hair plexuses are a specialized type of free nerve ending. They are coiled around
hair follicles, where they respond to movement of the hair.
Lamellated Corpuscles
Lamellated (pacinian) corpuscles are large, onion-shaped receptors composed of the
dendritic endings of several sensory nerve fibers enclosed by connective tissue layers.
They are commonly found within the synovial membranes of synovial joints, in the
perimysium of skeletal muscle tissue, and in certain visceral organs. Lamellated
corpuscles are also abundant in the skin of the palms and fingers of the hand, soles of
the feet, external genitalia, and breasts. They respond to heavy pressures, generally
those that are constantly applied. They can also detect deep vibrations in tissues and
organs.
Organs of Ruffini
The organs of Ruffini are encapsulated nerve endings that are found in the deep layers
of the dermis and in subcutaneous tissue, where they respond to deep continuous
pressure and to stretch. They are also present in joint capsules and function in the
detection of joint movement.
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Bulbs of Krause
The bulbs of Krause are thought to be a variation of Meissner’s corpuscles. They are
most abundant in the mucous membranes, and therefore are sometimes called
mucocutaneous corpuscles. Historically, both the organs of Ruffini and the bulbs of
Krause have been considered to be thermoreceptors—the former heat receptors and
the latter cold receptors. However, both are actually mechanoreceptors. The bulbs of
Krause respond to light pressure and low-frequency vibration. Any mother can attest to
the calming effect that holding and patting have on a crying baby. It has been known
that the touch of massage can relieve pain and improve concentration. There is now
evidence that touching and caressing newborns actually enhance their development.
Massaged infants gain weight nearly 50% faster than unmassaged infants. They are also
more active, alert, and responsive. Even premature infants grow and mature faster if
they are regularly held and touched.
Experiments with rats have shown that licking and grooming by the mother stimulate
the secretion of growth hormones in her pups (young). The amount of growth hormone
is significantly reduced in isolated pups that are not licked or groomed. Isolated pups
that are stroked periodically with a paintbrush, however, have normal secretion of
growth hormone.
THERMAL SENSATIONS
Thermal Receptors and Their Excitation
The human being can perceive different gradations of cold and heat, from freezing cold
to cold to cool to indifferent to warm to hot to burning hot.
Thermal gradations are discriminated by at least three types of sensory receptors: cold
receptors, warmth receptors, and pain receptors. The pain receptors are stimulated only
by extreme degrees of heat or cold and, therefore, are responsible, along with the cold
and warmth receptors, for "freezing cold" and "burning hot" sensations.
The cold and warmth receptors are located immediately under the skin at discrete
separated spots. In most areas of the body, there are 3 to 10 times as many cold spots
as warmth spots, and the number in different areas of the body varies from 15 to 25
cold spots per square centimeter in the lips to 3 to 5 cold spots per square centimeter in
the finger to less than 1 cold spot per square centimeter in some broad surface areas of
the trunk.
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Although the existence of distinctive warmth nerve endings is quite certain, based on
psychological tests, they have not been identified histologically. They are presumed to
be free nerve endings, because warmth signals are transmitted mainly over type C nerve
fibers at transmission velocities of only 0.4 to 2 m/sec.
Conversely, a definitive cold receptor has been identified. It is a special, small type Aδ
myelinated nerve ending that branches a number of times, the tips of which protrude
into the bottom surfaces of basal epidermal cells. Signals are transmitted from these
receptors via type Aδ nerve fibers at velocities of about 20 m/sec. Some cold sensations
are believed to be transmitted in type C nerve fibers as well, which suggests that some
free nerve endings also might function as cold receptors.
Stimulatory Effects of Rising and Falling Temperature-Adaptation of Thermal
Receptors
When a cold receptor is suddenly subjected to an abrupt fall in temperature, it becomes
strongly stimulated at first, but this stimulation fades rapidly during the first few
seconds and progressively more slowly during the next 30 minutes or more. In other
words, the receptor "adapts" to a great extent, but never 100 per cent.
Thus, it is evident that the thermal senses respond markedly to changes in temperature,
in addition to being able to respond to steady states of temperature. This means that
when the temperature of the skin is actively falling, a person feels much colder than
when the temperature remains cold at the same level. Conversely, if the temperature is
actively rising, the person feels much warmer than he or she would at the same
temperature if it were constant. The response to changes in temperature explains the
extreme degree of heat one feels on first entering a tub of hot water and the extreme
degree of cold felt on going from a heated room to the out-of-doors on a cold day.
Transmission of Thermal Signals in the Nervous System
In general, thermal signals are transmitted in pathways parallel to those for pain signals.
On entering the spinal cord, the signals travel for a few segments upward or downward
in the tract of Lissauer and then terminate mainly in laminae I, II, and III of the dorsal
horns-the same as for pain. After a small amount of processing by one or more cord
neurons, the signals enter long, ascending thermal fibers that cross to the opposite
anterolateral sensory tract and terminate in both (1) the reticular areas of the brain
stem and (2) the ventrobasal complex of the thalamus.
A few thermal signals are also relayed to the cerebral somatic sensory cortex from the
ventrobasal complex. Occasionally a neuron in cortical somatic sensory area I has been
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found by microelectrode studies to be directly responsive to either cold or warm stimuli
on a specific area of the skin. However, removal of the entire cortical postcentral gyrus
in the human being reduces but does not abolish the ability to distinguish gradations of
temperature.
Spatial Summation of Thermal Sensations
Because the number of cold or warm endings in any one surface area of the body is
slight, it is difficult to judge gradations of temperature when small skin areas are
stimulated. However, when a large skin area is stimulated all at once, the thermal
signals from the entire area summate. For instance, rapid changes in temperature as
little as 0.01°C can be detected if this change affects the entire surface of the body
simultaneously. Conversely, temperature changes 100 times as great often will not be
detected when the affected skin area is only 1 square centimeter in size.
SENSE OF EQUILIBRIUM
Equilibrium is maintained in response to two kinds of motion:
1. Static equilibrium maintains the position of the head in response to linear
movements of the body, such as starting to walk or stopping.
2. Dynamic equilibrium maintains the position of the head in response to rotational
motion of the body, such as rocking (as in a boat) or turning.
The perception of equilibrium occurs in the vestibular apparatus, which consists of the
vestibule and the semicircular canals. Motion in these two structures is detected as
follows:
 The vestibule is the primary detector of changes in static equilibrium. A sensory
receptor called a macula is located in the walls of the saccule and utricle, the two
bulblike sacs of the vestibule. A macula contains numerous receptor cells called hair
cells, from which numerous stereocilia (long microvilli) and a single kinocilium (a true
cilium) extend into a glycoprotein gel, the otolithic membrane. Calcium carbonate
crystals called otoliths pervade the otolithic membrane, increasing its density and
thus responsiveness to changes in motion. Changes in linear motion cause the
otolithic membrane to move forward and backward in the utricle or up and down in
the saccule. The movement of the otolithic membrane causes similar movements in
the embedded stereocilia of the hair cells, which in turn initiate graded potentials.
 The semicircular canals are the primary detector of changes in dynamic equilibrium.
The three canals, individually called the anterior, posterior, and lateral canals, are
arranged at right angles to one another. The expanded base of each canal, called an
ampulla, contains a sensory receptor, or crista ampullaris. Like the maculae of the
vestibule, each crista contains numerous hair cells whose stereocilia and kinocilium
protrude into a gelatinous matrix, the cupula (which is analogous to the otolithic
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membranes of the maculae). Changes in rotational motion cause the cupula and the
embedded stereocilia to move, which stimulates the hair cell to generate a graded
potential.
Graded potentials in the hair cells of the maculae and cristae result in changes in the
amounts of neurotransmitter secreted. In response to these changes, action potentials
are generated in the fibers of the vestibular nerve, which subsequently joins the
vestibulocochlear nerve. From here, the nerve impulses travel to the pons and the
cerebellum.
PROPRIOCEPTION
Proprioceptors monitor our own movements (proprius means “one’s own”) by
responding to changes in stretch and tension, and by transmitting action potentials to
the cerebellum. Proprioceptor information is then used to adjust the strength and
timing of muscle contractions to produce coordinated movements. Some of the sensory
impulses from proprioceptors reach the level of consciousness as the kinesthetic sense,
by which the position of the body parts is perceived. With the kinesthetic sense, the
position and movement of the limbs can be determined without visual sensations, such
as when dressing or walking in the dark. The kinesthetic sense, along with hearing,
becomes keenly developed in a blind person. High-speed transmission is a vital
characteristic of the kinesthetic sense because rapid feedback to various body parts is
essential for quick, smooth, coordinated body movements.
Proprioceptors are located in and around synovial joints, in skeletal muscle, between
tendons and muscles, and in the inner ear. They are of four types: joint kinesthetic
receptors, neuromuscular spindles, neurotendinous receptors, and sensory hair cells.
• Joint kinesthetic receptors are located in synovial joint capsules, where they are
stimulated by changes in body position as the joints are moved.
• Neuromuscular spindles are located in skeletal muscle, particularly in the muscles of
the limbs. They consist of the endings of sensory neurons that are spiraled around
specialized individual muscle fibers. Neuromuscular spindles are stimulated by an
increase in muscle tension caused by the lengthening or stretching of the individual
fibers, and thus provide information about the length of the muscle and the speed of
muscle contraction.
• Neurotendinous receptors (Golgi tendon organs) are located where a muscle attaches
to a tendon. They are stimulated by the tension produced in a tendon when the
attached muscle is either stretched or contracted.
• Sensory hair cells of the inner ear are located in a fluid-filled, ductule structure called
the membranous labyrinth.
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MODULE 2
MUSCLES AND GLANDS
Muscle enables complex movements that are either under conscious control, such as
turning the pages of a book, or involuntary, such as the contraction of the heart or the
peristalsis in the gut. The three types of muscles found in the human body are skeletal
(striated) muscles, cardiac muscles and smooth muscles.
Striated muscle
All movement is the result of the contraction of muscles. The muscles that we feel under
our skins, as well as many internal muscles that we cannot feel, such as the extraocular
muscles that move the eyeballs, are made of contractile tissue called skeletal or striated
muscle. A muscle is a bundle of numerous muscle fibers. Each muscle fiber is a single
long cell, and the cells in skeletal muscle are arranged parallel to each other, but are
separate. Within each fiber are numerous myofibrils, which run the full length of the
fiber. The name ‘striated muscle’ comes from the striped appearance that skeletal
muscle has under the microscope. The stripes consist of a number of bands and lines in
each myofibril. Each set of bands and lines is a functional unit called a sarcomere. A
sarcomere is composed of intersecting filaments made of proteins called actin and
myosin.
When a muscle is stimulated, a contraction occurs as a result of the actin filaments at
each end of a sarcomere being pulled into the central myosin filaments. This shortens
the muscle, and is called muscular contraction.
Within each muscle are subsets of fibers, which are innervated by a single motor
neuron. The motor neuron and the subset of fibers are together called a motor unit.
Muscles that control fine movements, such as those controlling the fingers and eye
movements, have small motor units (i.e. with few muscle fibers in each). Muscles that
control gross movements such as the biceps controlling flexion of the elbow, have larger
motor units. Skeletal muscles do not contract in an all-or-none manner. Stronger
contraction of a muscle results from the firing of more motor neurons and hence the
recruitment of more motor units.
Many muscles or muscle groups form opposed pairs with other muscles. Thus, for
example, the biceps, which flexes the elbow, is opposed by the triceps, which extends it.
Neural control of skeletal muscle
Muscles are controlled by motor neurons. When the motor neuron reaches the muscle
it branches, innervating the fibers of its motor unit. Between the end of each branch of
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the neuron and the muscle fiber it innervates is a type of synapse. Acetylcholine acts as
the neurotransmitter, and attaches to receptors on the motor endplate of the muscle
fiber. This starts an action potential, which in turn causes muscle contraction through
the myosin–actin mechanism described earlier. Each motor neuron leaves the ventral
horn of the spinal cord, although, there are two main sources of stimulation of motor
neurons.
Each muscle contains intrafusal muscle fibers, also called muscle spindles, which are
stretch receptors. When a muscle is stretched by contraction of an opposing muscle, the
afferent nerve fiber serving each spindle passes information to the spinal cord. Stretch
receptors in the tendons which attach muscles to bones, the Golgi tendon organs, also
serve as stretch detectors, passing afferent signals to the spinal cord. However, whereas
intrafusal fibers respond to passive stretch of the muscle, Golgi tendon organs respond
proportionally to the tension in the muscle. Both types of receptor are involved in the
reflexes we examine next.
Reflexes
While much of our muscular activity is controlled by the brain, many very important
muscle movements are controlled by spinal reflexes.
Reflexes are actions that take place automatically in response to some stimulus, and
permit immediate actions without the intervention of the brain. The simplest reflex is
the monosynaptic stretch reflex. The best-known example of this is the patellar reflex;
the knee jerk used by physicians to test the activity of spinal nerves. In this example,
striking the tendon below the knee cap (patella) stretches the quadriceps, the extensor
muscle in the front of the thigh. Stretching the muscle stimulates the muscle spindles.
Sensory neurons from the muscle spindles enter the dorsal root of the spinal cord, and
synapse with motor neurons in the ventral root, which causes the muscle to contract.
The normal function of this reflex is to cause a quick adjustment of muscle contraction
when the load on the muscle is increased. It acts as a continuous feedback loop
matching muscular contraction to the load on the muscle.
Polysynaptic reflexes are spinal reflexes that involve more than one synapse. An
example is the withdrawal or flexion reflex, when a limb is rapidly removed from a
painful stimulus. In this reflex, pain receptors send signals along axons to the dorsal root
of the spinal cord. These axons synapse with a number of short interneurons. These
interneurons connect with several motor neurons, producing a coordinated withdrawal
of the affected part of the body. However, some of the interneurons connect with
motor neurons on the other side of the body, where they produce limb extension: the
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crossed extensor reflex. The importance of this is that if, for example, you stand on a
pin, the resulting reflex withdrawal of that foot will be compensated by greater support
in the other leg.
Another type of reflex results from reciprocal innervation. This allows opposed groups
of muscles to organize their contraction and relaxation, permitting coordinated actions
such as walking. The simplest form of reciprocal innervations is when the flexor and
extensor muscles around a joint work together. In walking, for example, the knee joint
bends because the quadriceps muscle relaxes as the hamstring muscle flexes. Notice
that this is not a sudden on–off action; contraction and relaxation are gradual and
coordinated. The use of both legs in walking involves this reciprocal innervation, and
also the alternation of the actions of the two legs by means of the crossed extensor
reflex. All of this occurs without the necessity for conscious intervention. The main
principles of reflexes were demonstrated around the end of the 19 th and beginning of
the 20th centuries by Charles Sherrington. He showed how, in many organisms, much
behavior is composed of chains of reflexes. With increasing encephalization these are
increasingly controlled by brain mechanisms.
Smooth muscle and cardiac muscle
The actions of many internal organs are carried out by smooth muscle. Smooth muscle
underlies many of the physiological changes. Amongst other places, smooth muscle is
found in:
 the walls of blood vessels, where it is responsible for their constriction and
dilation. This permits fine control of blood flow to different tissues and organs;
 the walls of the intestines, where it is responsible for the contractions, called
peristalsis, which move food through the gastrointestinal tract;
 the sphincters that control filling and emptying of the gastrointestinal tract
and the genitourinary tract;
 the iris and the lens muscles within the eye;
 the hair follicles of the skin, where it produces piloerection (raising of the
hairs) in response to cold.
Generally, smooth muscle reacts slowly to stimulation, and produces mostly longerlasting changes. Smooth muscle is innervated by both branches of the autonomic
nervous system, which have opposing actions. As demands on the body vary, the
parasympathetic and sympathetic nervous systems vary the contraction of the smooth
muscle, matching the state of the organ to those demands.
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Cardiac, or heart, muscle is a specialized tissue that causes the heart to contract (beat),
pumping blood through the blood vessels. It, too, is controlled by opposing actions of
both branches of the autonomic nervous system.
CONTROL OF MOVEMENT BY THE BRAIN
Motor Cortex
Individual movements are controlled by the primary motor cortex. This occupies the
precentral gyrus, parallel to the somatosensory cortex in the postcentral gyrus. Penfield
and Rasmussen (1950) showed how each part of the body is controlled by a separate
area of the motor cortex, and parts capable of the most precise movements (especially
the fingers and lips) have larger areas of cortex devoted to them.
There are direct connections between neurons in the somatosensory cortex and in the
motor cortex that serve the same parts of the body. Evarts (1974), recording from the
primary motor cortex of monkeys, showed that tactile stimulation of the hand produces
very rapid responses in corresponding motor neurons, presumably by way of these
connections.
The main inputs to the primary motor cortex come from the premotor cortex and the
supplementary motor area located in the gyrus anterior to the primary motor cortex.
Together, these are sometimes called the secondary motor cortex. Their function seems
to be to produce movement programs: coordinated sets of movements. Through
numerous connections with the primary motor cortex, these motor programs control
individual movements, and produce coordinated behavior. Studies using PET scans in
humans have shown that the primary and secondary motor cortices, as well as the
primary somatosensory cortex, are all active both during performance of well-learned
response sequences and while learning new sequences (Jenkins et al., 1994). In
addition, during the learning of new sequences, but not during well-practiced ones, part
of the prefrontal cortex is active. Together with lesion studies, this suggests that the
planning of more complex behavior, or the construction of motor programs, takes place
in the prefrontal cortex.
The prefrontal cortex and the secondary motor cortex both receive inputs from areas of
association cortex involved with sensory and spatial information processing. Lesions in
the primary motor cortex produce paralysis of particular muscles or muscle groups.
However, lesions in the other areas involved in movement produce a variety of
apraxias: disorders of skilled movement not due to sensory loss or paralysis. For
example, patients may be unable to walk smoothly or follow instructions to move their
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legs (limb apraxia). In construction apraxia a person may be unable to make the
coordinated movements necessary to copy simple designs or complete a jigsaw puzzle.
Motor pathways
The contraction of muscles is controlled by motor neurons in the ventral roots of the
spinal cord. The pathways by which the brain controls these motor neurons are
complex, and what follows is a simplification.
The pyramidal system
One major pathway is the pyramidal system. In one part of this, the corticospinal
tract, axons from cortical neurons pass through the brain stem and down the spinal cord
before synapsing with motor neurons. Most of these axons decussate (cross to the other
side) in the brain stem, the remainder do so in the part of the spinal cord where their
target motor neurons are located. The other part of the pyramidal system, the
corticobulbar tract, passes to the medulla where it reaches the nuclei of various cranial
nerves.
Most of the neurons originate in large pyramidal cells in the primary motor cortex,
although many originate in the primary somatosensory cortex, and some in association
areas such as the premotor cortex. Some axons in the pyramidal tract end in various
sensory nuclei in the brain stem and spinal cord, and in the reticular formation.
Historically, the pyramidal system was characterized as the pathway by which voluntary
action is controlled; lesions confined to the pyramidal system cause paralysis of
voluntary movement, while many reflexes remain intact. However, the separation of
voluntary and automatic control is not actually this simple. Axons from the primary
motor cortex also pass to the basal ganglia and to the cerebellum, historically
considered to be involved with non-voluntary movement, both of which then feed back
to the primary and secondary motor cortex. The sensory connections indicate the
reliance of voluntary movement on immediate sensory feedback.
The extrapyramidal system
The other motor pathways have collectively been called the extrapyramidal system,
and characterized as involved in automatic (non-voluntary) movement. Lesions in these
tracts do not cause the loss of particular movements. Rather, patients show a variety of
difficulties involving either excessive movements that interfere with voluntary actions,
or slowed or limited movement that interferes with both voluntary and involuntary
movements. A number of tracts carry this sort of motor information, including the
vestibulospinal tracts, which originate in the brain stem, and influence the tone of limb
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muscles. They receive inputs from the vestibular system, and help to control posture
and maintain eye position. The rubrospinal tract has its origin in the red nucleus high in
the brain stem. This receives inputs from the primary motor cortex and from the
cerebellum. The rubrospinal tract connects to motor neurons of the major limb muscles,
so is involved in locomotion. The reticulospinal tracts originate in the reticular
formation of the brain stem. Their functions are not well understood, but they promote
certain reflexes, and help control automated actions such as walking and maintaining
posture.
As we have said, we cannot fully separate voluntary and involuntary components of the
motor system. The whole system is one in which automatic and voluntary pathways are
integrated with each other and with sensory mechanisms.
The basal ganglia
The basal ganglia are a group of interconnected subcortical nuclei. They include the
caudate nucleus and the putamen (together called the striatum), the globus pallidus,
the substantia nigra and the subthalamic nucleus. The striatum receives inputs from
many parts of the cerebral cortex, particularly the primary motor cortex and the primary
somatosensory cortex. In turn, the striatum projects to the globus pallidus, and has twoway connections with the substantia nigra. The globus pallidus has two-way connections
with the subthalamic nucleus, and projects to the secondary and primary motor cortices
by way of the thalamus. The functions of the basal ganglia are not fully worked out. In
general, their effect is inhibitory on the thalamus and hence on the cortex. Destruction
of parts of the basal ganglia causes characteristic, serious motor disorders.
Parkinson’s disease is a condition characterized by movement disorders including a
tremor when not trying to move, slowness, and difficulty starting movements. The cause
of Parkinson’s disease is degeneration of dopaminergic neurons in the substantia nigra,
which prevents information passing back to the striatum. Parkinson’s disease is treated
by large doses of L-dopa (‘Levodopa’), a precursor of dopamine. This passes into the
brain and into the remaining neurons in this circuit, enabling them to produce more
dopamine to affect the striatum.
Huntington’s chorea is a hereditary disease producing uncontrollable jerky movements
of the face and limbs. It results from degeneration of the striatum, particularly of
GABAergic neurons.
It is becoming clear that the basal ganglia are also involved in emotion. For example,
Schneider et al. (2003) have shown that electrical stimulation of the subthalamic
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nucleus, used as a treatment for long-term sufferers from Parkinson’s disease, increases
their sense of well-being and improves their emotional memory.
The cerebellum
The cerebellum is a relatively large structure located in the hindbrain. It contains more
neurons than the cerebral cortex, and structurally has several deep cerebellar nuclei
surrounded by a cortex. The cerebellum receives inputs from the motor cortex, from the
vestibular system from the special senses and from the somato-sensory system. Its
outputs go to motor centers in the extrapyramidal system. Damage to the cerebellum
causes serious deficits in the ability to produce smooth movement, including an
‘intention tremor’ which contrasts with the resting tremor of Parkinson’s disease. Other
symptoms can include muscle weakness, lack of coordination, slurring of speech, and a
staggering gait (ataxia). These all suggest that the cerebellum plays a key role in
programming sequential behaviors, especially those requiring integration of external
stimuli and timing. The cerebellum is involved in motor learning (Ohyama et al., 2003).
More recent studies have suggested that the cerebellum is important in emotional and
cognitive processes. For example, Leroi et al. (2002) reported very high rates of
psychiatric illness in patients with cerebellar disease.
The brain stem
A large class of behaviors that fall between the intentional, voluntary movements
controlled by the cerebral cortex and the reflexes controlled by the spine are
programmed by various centers in the brain stem. These behaviors include the
automatic processes controlled by the extrapyramidal system, such as postural changes,
eye movements, breathing, walking and the like. They also include more complex,
species-typical sequences of behavior that serve basic biological needs. Such
preprogrammed sequences can be seen in domestic animals — for example, the
stereotypical posture and movements of a hunting cat.
For some of these behaviors in other species, control centers have been identified in
various parts of the brain stem. For example, a region of the periaqueductal gray (PAG)
produces sexual receptive behavior in female rodents. Note that, although these
species-typical behaviors are preprogrammed, they are not necessarily inevitable. They
are responsive both to sensory inputs and to conscious modification. They are
responsive both to sensory inputs and to conscious modification.
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HORMONES AND THEIR ACTION
What is a hormone?
The hormone or endocrine system provides, generally, a slower means of control over
the functions of the body than the nervous system. Like neurotransmitters, hormones
are specialized chemicals that change the activity of cells by attaching to receptors on
the cells. To emphasize the close relationships we will see between hormones and the
actions of the nervous system, the endocrine system is sometimes referred to as the
neuroendocrine system. Most hormones are released from specialized endocrine
glands, and the rest from special cells within organs like the kidney and stomach.
Wherever the hormone is released from, it usually travels to its target through the
bloodstream.
Hormones fall mainly into four different groups of chemicals. These are:
1. peptides and proteins;
2. amino acids;
3. fatty acids;
4. steroids.
The peptides and proteins exhibit a wide variety of sizes and shapes of molecule and
include insulin. The amino acids include the thyroid hormones such as thyroxine, and
epinephrine, which is derived from tyrosine. The fatty acids include the prostaglandins
and are made from polyunsaturated fats. Finally, the steroids include testosterone and
are derived from cholesterol. These subdivisions are sometimes simplified into steroids
and non-steroids.
Where do hormones act?
Hormones mostly travel in the bloodstream where they come into contact with all cells.
However, they only have an effect once they reach their own target cells. These cells
have specially adapted receptors that accept the hormone in the same ‘lock and key’
fashion that for neurotransmitters. A target cell may be receptive to just one particular
hormone or to a number of different hormones. For each hormone, though, there is a
specific receptor site.
Most hormones travel in the bloodstream to affect a distant target organ. However,
some act more locally, or even on the very cell that secreted it. To differentiate between
these actions the term endocrine action is used to describe a distant action, paracrine
action is used to describe a more localized action, and autocrine action is used to
describe a hormone that acts on the cells that released it.
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Another noteworthy feature of hormones is their speed of action. When a neuron fires,
its effects are virtually immediate as conduction is fast and the neurotransmitter
substance is, to all intents and purposes, instantaneously released. By contrast, when a
hormone is released it must usually travel in the bloodstream until it reaches its target
destination. Add to this the fact that the release of the required hormone is sometimes
only triggered by another hormone also released into the bloodstream, and the time it
takes for the required hormone to finally exert its effect on the target organ can be of
the order of a few minutes. Compare, for example, the speed with which you remove
your hand from a hot object (neuronal) with the time it takes to induce milk ejection
from a stimulated nipple (30–60 seconds).
Direct integration between endocrine activity and activity of the nervous system is
achieved by a group of chemicals called neurohormones. These are released by the
endocrine system but have their targets in the nervous system. For example,
cholecystokinin (CCK) is released by the small intestine and acts on certain brain stem
nuclei. Similarly, epinephrine is released into the bloodstream by the adrenal gland and
travels to the neurons of the sympathetic nervous system where it causes the
sympathetic arousal.
Positive and negative feedback
The amount of a hormone that is present in the blood is crucial for the effective working
of the endocrine system. Hormonal action needs a monitoring system so that the
amount of hormone can be increased or reduced as necessary. Most hormonal control
is by negative feedback. The cells that initially release the hormone are receptive to the
presence of the hormone in the blood. As more and more of the hormone is released,
the quantity in the blood rises. At some cut-off point, the receptorswithin the endocrine
gland register that there is enough hormone circulating and turn off production and/or
release of any more hormone. For some hormones, there is more than one place at
which such monitoring occurs.
In a few cases, the feedback system is positive. Here, the detection of the presence of
the hormone in the blood triggers even more to be released. An example of this is the
hormone oxytocin, released from the posterior pituitarygland. This stimulates milk
secretion from the breast. The act of suckling stimulates the release of oxytocin and is a
positive feedback mechanism.
Major Endocrine Glands of Human Body
The Pituitary Gland
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The pituitary gland has two main parts, anterior and posterior. Both have a vascular link
with the hypothalamus, and the posterior pituitary has a neural connection with it. They
are responsible for the release of different hormones and stimulating hormones.
Most of the hormones that circulate around the body are controlled in one way or
another by the pituitary gland.
The hypothalamus controls hormonal release. It does so mainly by influencing the
release of hormones and stimulating hormones from the pituitary gland. However,
control of the anterior pituitary is by hormones released by the hypothalamus but the
posterior pituitary is controlled by neuronal input from the hypothalamus.
The posterior pituitary gland secretes just two hormones, oxytocin and vasopressin. The
former is involved in lactation and the latter is involved in blood pressure control.
Most of the hormones released by the anterior pituitary are stimulating hormones.
These stimulate other glands to release their hormones into the blood. The exception
here is prolactin which is a hormone that acts directly on target cells.
The Adrenal Glands
The adrenal glands are located above the kidneys and consist of an outer layer
called the adrenal cortex and an inner core called the adrenal medulla. The medulla is
made up of chromaffin cells that release epinephrine and norepinephrine when
stimulated. These are released as part of the stress response. The adrenal cortex
secretes three different kinds of hormones, the glucocorticoids, the mineralocorticoids
and the sex steroids. The corticoids are involved in metabolism and the sex steroids are
involved in secondary sexual characteristics.
The Pancreas
The pancreas is located at the back of the abdomen. It has cells called Islets of
Langerhans that secrete its hormones into the blood. The pancreas secretes insulin and
glucagon to regulate the levels of blood glucose and the storage of fats. Somatostatin is
also secreted, and helps to control the secretion of insulin and glucagon.
The Thyroid Gland
The thyroid gland is located in the throat just below the Adam’s apple. It has a butterfly
shape and secretes two hormones that regulate metabolism and have an effect in nearly
all parts of the body. The parathyroid gland is located in the front of the neck, close to
the thyroid gland. It is actually made up of four small glands.
The thyroid gland secretes thyroxine and triiodothyronine (involved in
metabolism), and calcitonin (involved in calcium regulation). The parathyroids secrete
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parathyroid hormone, which is responsible for regulating the levels of calcium and
phosphate in the blood.
The Ovaries
The ovaries are oblong organs that lie in the pelvis at the ends of the fallopian tubes. As
well as egg production, they secrete a number of hormones. The testes are glandular
organs that are suspended in the scrotum. As well as producing sperm, they secrete a
number of hormones.
The ovaries produce estrogens and the progestins. Estrogens are involved in
development, especially of the reproductive system. They are not exclusively female
hormones. Progestins are concerned with reproduction itself. The testes secrete
androgens, and in particular, testosterone. Testosterone is an important hormone for
sexual development in the male.
Other Glands and Hormones
The thymus hormone secreted by thymus gland is responsible for cellular immunity.
Most of its job is done shortly before birth and for a short period afterwards.
The kidneys secrete three different hormones; renin, erythropoietin and 1,25dihydroxy-vitamin D3. These have a role in blood pressure, erythrocyte production and
calcium balance respectively.
The pineal gland secretes melatonin. This has been strongly linked with the sleep–
waking cycle. It also has a role in seasonal breeding and sexual maturity.
There are several hormones secreted by the gastrointestinal tract. They include gastrin,
secretin, cholecystokinin, gastric inhibitory peptide and somatostatin.
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