Bio Psy Chapter 6 10

Jose Rizal University
Mandaluyong City
College of Liberal Arts, Criminology and Education

Department of Psychology
BIOLOGICAL PSYCHOLOGY
CHAPTER 6: VISION
Chapter Outline
A. General Principles of Perception

a. Each of our senses has specialized receptors that are sensitive to a particular
kind of energy
b. Receptors for vision are sensitive to light
c. Receptors “transduce” (convert) energy into electrochemical patterns so that
the brain can perceive sights, sounds, smells, etc.
d. Law of specific nerve energies states that activity by a particular nerve always
conveys the same type of information to the brain. Example: impulses in one
neuron indicate light; impulses in another neuron indicate sound
e. Which neurons respond, the amount of response, and the timing of response
influence what we perceive
B. The Eye and Its Connections to the Brain

a. Light enters the eye through an opening in the center of the iris called the
pupil
b. Light is focused by the lens and the cornea onto the rear surface of the eye
known as the retina
i. The retina is lined with visual receptors
c. Light from the left side of the world strikes the right side of the retina and vice
versa
d. Visual receptors send messages to neurons called bipolar cells, located closer
to the center of the eye
e. Bipolar cells send messages to ganglion cells that are even closer to the
center of the eye
f. The axons of ganglion cells join one another to form the optic nerve that
travels to the brain
g. Amacrine cells are additional cells that receive information from bipolar cells
and send it to other bipolar, ganglion, or amacrine cells. Amacrine cells
control the ability of the ganglion cells to respond to shapes, movements, or
other specific aspects of visual stimuli
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h. The optic nerve consists of the axons of ganglion cells that band together and
exit through the back of the eye and travel to the brain
i. The point at which the optic nerve leaves the back of the eye is called the blind
spot because it contains no receptors
j. The central portion of the retina is the fovea and allows for acute and detailed
vision
i. Packed tight with receptors
ii. Nearly free of ganglion axons and blood vessels
k. Each receptor in the fovea attaches to a single bipolar cell and a single
ganglion cell known as a midget ganglion cell
l. Each cone in the fovea has a direct line to the brain which allows the
registering of the exact location of input
m. Our vision is dominated by what we see in the fovea
n. In the periphery of the retina, a greater number of receptors converge into
ganglion and bipolar cells
i. Detailed vision is less in peripheral vision
ii. Allows for the greater perception of much fainter light in peripheral
vision
o. The arrangement of visual receptors in the eye is highly adaptive
i. Example: predatory birds have a greater density of receptors on the
top of the eye; rats have a greater density on the bottom of the eye
C. Visual Receptors: Rods and Cones

a. The vertebrate retina consists of two kinds of receptors:
i. Rods: most abundant in the periphery of the eye and respond to faint
light (120 million per retina)
ii. Cones: most abundant in and around the fovea (6 million per retina)
1. Essential for color vision & more useful in bright light
b. Though cones are outnumbered, they provide about 90% of the brain’s input
c. The average number of axons in the optic nerve is one million, but some
people may have two or three times as many
d. Heightened visual responses are important in many activities
i. Example: top tennis, squash, and fencing athletes show faster brain
responses to visual stimuli
e. Photopigments: chemicals contained by both rods and cones that release
energy when struck by light
i. Consist of 11-cis-retinal bound to proteins called opsins
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f. Light energy converts 11-cis-retinal quickly into all-trans-retinal
g. Light is thus absorbed and energy is released that activates second
messengers within the cell
D. Color Vision
a. The perception of color is dependent upon the wavelength of the light
b. “Visible” wavelengths are dependent upon the species’ receptors
c. The shortest wavelength humans can perceive is 400 nanometers (violet)
d. The longest wavelength that humans can perceive is 700 nanometers (red)
e. Discrimination among colors depend upon the combination of responses by
different neurons
f. Two major interpretations of color vision include the following:
i. Trichromatic theory/Young-Helmholtz theory - color perception occurs
through the relative rates of response by three kinds of cones
1. Short wavelength, medium-wavelength, long-wavelength
2. Each cone responds to a broad range of wavelengths, but some
more than others
3. The ratio of activity across the three types of cones determines
the color
4. More intense light increases the brightness of the color but does
not change the ratio
5. Incomplete theory of color vision. Example: negative color
afterimage
ii. Opponent-process theory - suggests that we perceive color in terms of
paired opposites
1. The brain has a mechanism that perceives color on a continuum
from red to green and another from yellow to blue
2. A possible mechanism for the theory is that bipolar cells are
excited by one set of wavelengths and inhibited by another
iii. Both the opponent-process and trichromatic theory have limitations
1. Color constancy, the ability to recognize color despite changes
in lighting, is not easily explained by these theories
2. Retinex theory suggests the cortex compares information from
various parts of the retina to determine the brightness and color
for each area
a. Better explains color and brightness constancy
g. Color vision deficiency is an impairment in perceiving color differences
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h. Gene responsible is contained on the X chromosome (~8% of men & <1% of
women)
i. Caused by either the lack of a type of cone or a cone has abnormal properties
j. Most common form is difficulty distinguishing between red and green
i. Results from the long- and medium- wavelength cones having the
same photopigment
E. An Overview of the Mammalian Visual System

a. Rods and cones of the retina make synaptic contact with horizontal cells and
bipolar cells
b. Horizontal cells are cells in the eye that make inhibitory contact onto bipolar
cells
c. Bipolar cells make synapses onto amacrine cells and ganglion cells
d. The different cells are specialized for different visual functions
e. Ganglion cell axons form the optic nerve
f. The optic chiasm is the place where the two optic nerves leaving the eye meet
g. In humans, half of the axons from each eye cross to the other side of the brain
h. Most ganglion cell axons go to the lateral geniculate nucleus, a smaller
amount to the superior colliculus, and fewer to other areas
F. The Neural Basis of Visual Perception

a. The lateral geniculate nucleus is part of the thalamus specialized for visual
perception
i. Destination for most ganglion cell axons
ii. Sends axons to other parts of the thalamus and to the visual areas of
the occipital cortex
iii. Cortex and thalamus feed information back and forth to each other
G. Processing in the Retina

a. Lateral inhibition is the reduction of activity in one neuron by activity in
neighboring neurons
b. The response of cells in the visual system depends upon the net result of
excitatory and inhibitory messages it receives
c. Lateral inhibition is the retina’s way responsible of sharpening contrasts to
emphasize the borders of objects
d. The receptive field refers to the part of the visual field that either excites or
inhibits a cell in the visual system of the brain
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e. For a receptor, the receptive field is the point in space from which light strikes
it
f. For other visual cells, receptive fields are derived from the visual field of cells
that either excite or inhibit
i. Example: ganglion cells converge to form the receptive field of the
next level of cells
g. Ganglion cells of primates generally fall into three categories:
i. Parvocellular neurons
1. Mostly located in or near the fovea
2. Have smaller cell bodies and small receptive fields
3. Are highly sensitive to detect color and visual detail
ii. Magnocellular neurons
1. Are distributed evenly throughout the retina
2. Have larger cell bodies and visual fields
3. Are highly sensitive to large overall pattern and moving stimuli
iii. Koniocellular neurons
1. Have small cell bodies
2. Are found throughout the retina
3. Have several functions, and their axons terminate in many
different places
h. Cells of the lateral geniculate have a receptive field similar to those of
ganglion cells:
i. An excitatory or inhibitory central portion and a surrounding ring of the
opposite effect
H. The Primary Visual Cortex

a. Pattern recognition in the cerebral cortex occurs in a few places
b. The primary visual cortex (area V1) receives information from the lateral
geniculate nucleus and is the area responsible for the first stage of visual
processing
c. Some people with damage to V1 show blindsight: an ability to respond to
visual stimuli that they report not seeing
d. Hubel and Weisel (1959, 1998) distinguished various types of cells in the
visual cortex:
i. Simple cells
1. Fixed excitatory and inhibitory zones
2. The more light that shines in the excitatory zone, the more the
cell responds
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3. The more in the inhibitory zone, the less the cell responds
4. Bar-shaped or edge-shaped receptive fields with vertical and
horizontal orientations outnumbering diagonal ones
ii. Complex cells
1. Located in either V1or V2
2. Have large receptive field that cannot be mapped into fixed
excitatory or inhibitory zones
3. Responds to a pattern of light in a particular orientation and
most strongly to a moving stimulus
iii. End-stopped/hypercomplex cells
1. Are similar to complex cells but with a strong inhibitory area at
one end of its bar shaped receptive field
2. Respond to a bar-shaped pattern of light anywhere in its large
receptive field, provided the bar does not extend beyond a
certain point
e. In the visual cortex, cells are grouped together in columns perpendicular to
the surface
f. Cells within a given column process similar information
i. Respond either mostly to the right or left eye, or respond to both eyes
equally
ii. Do not consistently fire at the same time
g. Cells in the visual cortex may be feature detectors, neurons whose response
indicate the presence of a particular feature/ stimuli
h. Prolonged exposure to a given visual feature decreases sensitivity to that
feature
I. Development of the Visual Cortex

a. Animal studies have greatly contributed to the understanding of the
development of vision
b. Early lack of stimulation of one eye: leads to synapses in the visual cortex
becoming gradually unresponsive to input from that eye
c. Early lack of stimulation of both eyes: cortical responses become sluggish but
do not cause blindness
d. Sensitive/critical periods are periods of time during the lifespan when
experiences have a particularly strong and enduring effect
e. Critical period ends with the onset of chemicals that inhibit axonal sprouting
f. Changes that occur during critical period require both excitation and
inhibition of some neurons
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g. Cortical plasticity is greatest in early life, but never ends
h. Stereoscopic depth perception is a method of perceiving distance in which
the brain compares slightly different inputs from the two eyes
i. Relies on retinal disparity or the discrepancy between what the left and the
right eye sees
j. The ability of cortical neurons to adjust their connections to detect retinal
disparity is shaped through experience
k. Strabismus is a condition in which the eyes do not point in the same direction
i. Usually develops in childhood
ii. Also known as “lazy eye”
l. If two eyes carry unrelated messages, cortical cell strengthens connections
with only one eye
m. Development of stereoscopic depth perception is impaired
n. Early exposure to a limited array of patterns leads to nearly all of the visual
cortex cells becoming responsive to only that pattern
o. Astigmatism refers to a blurring of vision for lines in one direction caused by
an asymmetric curvature of the eyes
i. 70% of infants have astigmatism
p. Study of people born with cataracts but had them removed at age 7 or 12
indicate that vision can be restored gradually, but problems persist:
i. Difficulty in recognizing objects
ii. Unable to tell that components are part of a whole
iii. Best prognosis is for children whose vision problems are corrected
early in life
J. The “What” and “Where” Paths

a. The secondary visual cortex (area V2) receives information from area V1,
processes information further, and sends it to other areas
b. Information is transferred between area V1 and V2 in a reciprocal nature
c. The ventral stream refers to the path that goes through temporal cortex; the
“what” path
i. Specialized for identifying and recognizing objects
d. The dorsal stream refers to the visual path in the parietal cortex; the “where”
path
i. Helps the motor system to find objects and move towards them
e. The two streams communicate
i. Each participates in identifying what and where an object is
f. Damaging either stream will produce different deficits
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i. Ventral stream damage: can see where objects are but cannot identify
them
ii. Dorsal stream damage: can identify objects but not know where they
are
K. Detailed Analysis of Shape

a. Receptive fields become larger and more specialized as visual information
goes from simple cells to later areas of visual processing
b. The inferior temporal cortex contains cells that respond selectively to complex
shapes but are insensitive to distinctions that are critical to other cells
c. Cells in this cortex respond to identifiable objects
d. Shape constancy is the ability to recognize an object’s shape despite changes
in direction or size
e. The inferior temporal neuron’s ability to ignore changes in size and direction
contributes to our capacity for shape constancy
f. Damage to the pattern pathways of the cortex can lead to deficits in object
recognition
g. Visual agnosia is the inability to recognize objects despite satisfactory vision
i. Caused by damage to the pattern pathway usually in the temporal
cortex
h. Face recognition occurs relatively soon after birth
i. People with cataracts removed at 2-6 months develop nearly normal vision
but have slight difficulties in distinguishing faces
j. Newborns show strong preference for a right-side-up face and support idea
of a built-in face recognition system
k. Facial recognition continues to develop gradually into adolescence
l. Prosopagnosia is the inability to recognize faces
i. Occurs after damage to the fusiform gyrus of the inferior temporal
cortex
ii. The fusiform gyrus responds much more strongly to faces than
anything else
L. Color Perception
a. Color perception depends on both the light reflected on an object and how
it compares with objects around it
i. Area V4 may be responsible for color constancy and visual attention
ii. Color constancy: the ability to recognize something as being the same
color despite changes in lighting
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M. Motor Perception
a. Motion perception involves a variety of brain areas in all four lobes of the
cerebral cortex
b. The middle-temporal cortex (MT/V5) responds to a stimulus moving in a
particular direction
c. Cells in the dorsal part of the medial superior temporal cortex (MST) respond
to expansion, contraction or rotation of a visual stimulus
d. Both receive input from the magnocellular path; color-insensitive
e. Motion blindness refers to the inability to determine the direction, speed and
whether objects are moving
i. Likely caused by damage in area MT
f. Some people are blind except for the ability to detect which direction
something is moving
i. Area MT probably gets some visual input despite significant damage
to area V1
g. Several mechanisms prevent confusion or blurring of images during eye
movements
i. Saccades are a decrease in the activity of the visual cortex during quick
eye movements
ii. Neural activity and blood flow decrease 75 ms before and during eye
movements
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CHAPTER 7: OTHER SENSORY SYSTEMS

Chapter Outline
I. Audition
A. Sound and the Ear

1. Physical and Psychological Dimensions of Sound
a. Sound waves are periodic compressions of air, water, or another
medium.
b. Sound waves vary in amplitude and frequency.
c. Amplitude: Intensity of a sound wave. Loudness is the perception of
intensity. Loudness is not always related to amplitude. Faster speaking
may cause sound louder even though it is the same amplitude.
d. Frequency: Number of compressions per second, measured in hertz
(Hz) of a sound.
e. Pitch: The perception of frequency (the higher the frequency of a
sound, the higher its pitch).
f. Most adult humans can hear vibrations from 15 to almost 20,000 Hz.
2. Structures of the Ear

a. The anatomy of the ear is described in terms of three regions: the
outer ear, the middle ear, and the inner ear.
b. The outer ear includes the pinna (structure of flesh and cartilage
attached to the side of the head) and the auditory canal. The pinna
helps us locate the source of a sound by altering reflections of sound
waves.
c. The middle ear is comprised of the tympanic membrane (eardrum),
which vibrates at the same frequency as the sound waves that strike it.
Sound waves reach the tympanic membrane through the auditory
canal. The tympanic membrane is attached to three tiny bones
(hammer, anvil, and stirrup).
d. The inner ear consists of the oval window, which receives vibrations
from the tiny bones of the middle ear, and the cochlea, which contains
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three fluid-filled tunnels: the scala vestibuli, scala media, and scala
tympani.
e. The stirrup causes the oval window to vibrate, setting in motion all the
fluid in the cochlea.
f. The auditory receptors (hair cells) lie between the basilar membrane
and the tectorial membrane in the cochlea.
g. When fluid in the cochlea vibrates, a shearing action occurs, which
stimulates hair cells; these cells then stimulate the auditory nerve cells
(eighth cranial nerve).
B. Pitch Perception
1. Frequency and Place
a. Place Theory: Each area along the basilar membrane is tuned to a
specific frequency and vibrates whenever that frequency is present.
Each frequency activates hair cells at only one place along the basilar
membrane, and the brain distinguishes frequencies by which neurons
are activated. This theory has a downfall in that various parts of the
basilar membrane are bound too tight for any part to resonate like a
piano string.
b. Frequency Theory: We perceive certain pitches when the basilar
membrane vibrates in synchrony with a sound, causing the axons of
the auditory nerve to produce action potentials at the same frequency.
c. The current theory combines modifications of both frequency and
place theories: For low frequency sounds (below 100 Hz), the basilar
membrane does vibrate in synchrony with the sound wave in
accordance with frequency theory. The pitch of the sound is identified
by the frequency of impulses and the loudness is identified by the
number of firing cells.
d. Volley principle of pitch discrimination: The auditory cortex as a whole
can have volleys of impulses up to about 4000 per second, even
though no individual axon approaches this frequency alone.
e. The volley principle is believed to be important for pitch perception
below 4000 Hz, although it is unclear how the brain uses this
information,
f. For high frequency sounds (above 5000 Hz), we use a mechanism
similar to place theory. High frequency vibrations strike the basilar
membrane, causing a traveling wave. This causes displacement of hair
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cells near the base (where the stirrup meets the cochlea). Low
frequency sounds produce displacement farther along the membrane.
g. Tone deafness or amusia: a disorder where individuals are seriously
impaired at detecting small changes in frequency. Many relatives of
those with amusia have the same condition. It is associated with a
thicker than average auditory cortex in the right hemisphere but fewer
than average connections from the auditory cortex to the frontal
cortex.
h. Absolute pitch or perfect pitch: the ability to hear a note and identify it
accurately. It is somewhat determined by genetic predisposition. The
main determinant is extensive musical training.
C. The Auditory Cortex

1. Auditory information passes through several subcortical structures with an
important crossover in the midbrain that enables each hemisphere of the
forebrain to get its major auditory input from the opposite ear.
2. Primary auditory cortex (area A1): Ultimate destination of auditory
information is located in the superior temporal cortex. Area A1 also is
important for auditory imagery. Similar to the visual system, the auditory
system needs experience to develop normally. Both constant noise and
lack of exposure to sound will impair the development of the auditory
system.
3. Damage to the A1 does not leave someone deaf; it may hinder the ability
to recognize combinations or sequences of sounds, like music or speech.
4. In the primary auditory cortex, cells respond preferentially to certain tones.
Cells preferring a given tone in the auditory cortex cluster together
providing a map of the sounds referred to as a tonotopic map. Thus, the
cortical area with the greatest response indicates what sound or sounds
are heard.
5. Cells outside area A1 respond best to auditory “objects” such as animal
cries, machinery noise, music, etc.
A. Hearing Loss
1. Conductive or middle-ear deafness: Failure of the bones of the middle ear
to transmit sound waves properly to the cochlea. Conductive deafness can
be caused by diseases, infections, or tumorous bone growth near the ear.
This deafness can be corrected by surgery or hearing aids.
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2. Nerve or inner-ear deafness: Damage to the cochlea, hair cells, or auditory
nerve that causes a permanent impairment in hearing in one to all ranges
of frequencies. Nerve deafness can be inherited or caused by prenatal
problems and early childhood disorders.
3. Tinnitus: Frequent or constant ringing in the ear. Tinnitus is often
produced by nerve deafness. It is a phenomenon similar to phantom limb,
where axons corresponding to other parts of the body may invade the
brain area previously responsive to sounds, especially high-frequency
sounds.
D. Sound Localization
1. Humans localize low frequency sounds by differences in phase. We
localize high frequencies by loudness differences. We can localize a sound
of any frequency by its time of onset, if the onset is sudden enough. Most
speech sounds are localized by differences in time of onset to each ear.
2. Adult humans are accurate at localization for frequencies above 2000 to
3000 Hz, and less accurate for progressively lower frequencies.
II. The Mechanical Senses
A. The mechanical senses include touch, pain, and other body sensations, as well
as vestibular sensation (specialized to detect the position and movement of
the head). They respond to pressure, bending, or other distortions of a
receptor.
B. Vestibular Sensation
1. The vestibular organ monitors head movements and directs
compensatory movements of the eyes. It is critical for eye movements and
maintaining balance.
2. The vestibular organ is comprised of two otolith organs (the saccule and
utricle) and three semicircular canals.
3. Calcium carbonate particles (otoliths) lie next to hair cells in the otolith
organs and excite them when the head tilts in different directions.
4. The three semicircular canals are filled with a jellylike substance and are
lined with hair cells. Acceleration of the head causes this substance to
push against hair cells, which in turn causes action potentials from the
vestibular system to travel via part of the eighth cranial nerve to the
brainstem and cerebellum.
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C. Somatosensation
1. The somatosensory system involves the sensation of the body and its
movements, including discriminative touch, deep pressure, cold, warmth,
pain, itch, tickle, and the position and movements of joints.
2. Somatosensory Receptors
a. Examples of touch receptors are pain receptors, Ruffini endings,
Meissner’s corpuscles, and Pacinian corpuscles.
b. Stimulation of touch receptors opens sodium channels in the axon,
possibly starting an action potential if the stimulation is strong
enough.
c. Pacinian corpuscle detects sudden displacements or high-frequency
vibrations on the skin.
d. Receptors for heat and cold can be stimulated by certain chemicals as
well as mechanical stimulation.
3. Input to the Central Nervous System
a. Somatosensory information from the head enters the CNS through the
cranial nerves. Information from touch receptors below the head
enters the spinal cord through the 31 spinal nerves and passes toward
the brain.
b. Each spinal nerve has a sensory component and a motor component.
Each sensory spinal nerve innervates a limited area of the body called
a dermatome.
c. Sensory information from the spinal cord is sent to the thalamus
before traveling to the somatosensory cortex in the parietal lobe.
d. The somatosensory cortex receives information primarily from the
contralateral side of the body.
e. Touch perception may differ from reality. The cutaneous rabbit
illusion: when someone taps you very rapidly six times on the wrist and
then three times near the elbow, you will have a sensation of
something like a rabbit hopping from the wrist to the elbow, with an
extra, illusory, stop in between.
f. Damage to the somatosensory cortex impairs body perceptions. A
patient with Alzheimer’s who exhibited such damage had trouble
putting her clothes on correctly.
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D. Pain:
1. Pain is the experience evoked by a harmful stimulus, directing our
attention towards danger.
2. Pain Stimuli and Pain Pathways
a. Receptors are bare nerve endings, some of which also respond to acid
and heat.
b. Capsaicin, a chemical found in hot peppers and jalapeños, also
stimulates pain receptors.
c. Pain conveyed over thin, slow, unmyelinated axons is experienced as
dull pain. Thicker and faster axons convey sharp pain.
d. Mild pain causes the release of the neurotransmitter glutamate in the
spinal cord, whereas strong pain causes the release of both glutamate
and substance P.
e. The pain signal ascends the contralateral spinal cord to the thalamus
and from there projects to the primary somatosensory cortex in the
parietal lobe.
f. Pain information also ascends to the reticular formation of the
medulla, where it projects to the limbic system to generate emotional
associations and memories.
3. Ways of Relieving Pain

a. Insensitivity to pain is dangerous. Those with the gene that inactivates
pain axons suffer from repeated injuries and generally fail to learn to
avoid dangers.
b. Opiods and Endorphins
i. Opiod Mechanisms: released by the brain to dull prolonged
pain after you are alerted of danger.
ii. Opiods bind to receptors in the spinal cord and periaqueductal
gray area to block the release of substance P and decrease
prolonged pain.
iii. Endorphins: the transmitters that attach to the same receptors
as morphine. Different endorphins (naturally released by the
brain) relieve different types of pain.
iv. Gate Theory: Information not related to pain travels to the
spinal cord and closes the “gates” for each pain message,
thereby modulating the subjective experience of pain.
Although gate theory turned out to be wrong, the general
principle is valid: nonpain stimuli modify the intensity of pain.
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c. Placebo: a drug that has no pharmacological effects, yet reduces the
perception of pain.
d. Cannabinoids and Capsaicin
i. Cannabinoid (chemical related to marijuana): blocks certain
kinds of pain through the periphery of the body rather than the
CNS
ii. Capsiacin: produces a painful burning sensation by releasing
substance P. This process exhausts the neurons’ production of
substance P, leaving the cells less able to send pain messages.
High doses of capsaicin damage pain receptors.
4. Sensitization of Pain
a. The body also has mechanisms to increase pain after tissue has been
damaged and inflamed.
b. Pain sensitization is a result of the body releasing histamine, nerve
growth factor, and other chemicals that are necessary to repair the
body.
c. Nonsteroidal anti-inflammatory drugs decrease pain by reducing the
release of chemicals from damaged tissue.
5. Social Pain
a. A romantic breakup can trigger emotional pain, which is similar in
many respects to physical pain.
b. Emotional pain is experienced in the cingulate cortex of the brain.
c. Emotional pain can be relieved by pain-relieving drugs like
acetaminophen (Tylenol).
E. Itch
1. Exists in two forms
a. In response to tissue damage, due to release of histamine
b. In response to contact with certain plants
2. Both forms are conveyed by a single spinal pathway that tends to be
slower than other tactile sensations.
3. Itch activates neurons in the spinal cord that produce a chemical called
gastin-releasing peptide.
4. Itch is useful because it directs you to scratch the itchy area and remove
whatever is irritating your skin.
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5. Vigorous scratching produces mild pain, and pain inhibits itch. Opiates
reduce pain and increase itch. The inhibitory relationship between pain
and itch is evidence that itch is not a type of pain.
III. The Chemical Senses
A. Chemical Coding
1. Labeled-line principle: Receptors of a sensory system that respond to a
limited range of stimuli and send a direct line to the brain.
2. Across-fiber pattern principle: Receptors of a sensory system respond to a
wide range of stimuli and contribute to the perception of each of them.
3. Vertebrate sensory systems probably do not have any pure labeled-line
codes. Taste and smell stimuli excite several kinds of neurons, and the
meaning of a particular response by a particular neuron depends on the
responses of other neurons.
B. Taste
1. Taste results from the stimulation of taste buds. Taste differs from flavor,
which is the combination of taste and smell. Taste and smell axons
converge into many of the same cells in an area called the endopiriform
cortex.
2. Taste Receptors
a. Taste receptors are actually modified skin cells that last only about 10-
14 days before being replaced.
b. Mammalian taste receptors are located in taste buds, which are
located in papillae (structures on the surface of the tongue). A given
papillae may contain from 0 to 10 taste buds and each taste bud
contains about 50 receptor cells.
c. In adult humans, taste buds are located mainly on the outside edge of
the tongue.
2. How Many Kinds of Taste Receptors?

a. We have long known of the existence of at least four types of “primary”
tastes: sweet, sour, salty, and bitter. Chemicals that alter one receptor
but not others have been used to identify taste receptor types.
b. Adaptation: Decreased response to a stimulus as a result of recent
exposure to it (e.g., if the tongue is soaked in two sour solutions, one
after the other, the second solution will not taste as sour as the first).
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c. Cross-adaptation: A reduced response to one taste because of
exposure to another. There is little cross-adaptation in taste.
d. Umami: A taste associated with glutamate. Researchers have found a
glutamate taste receptor responsible for this fifth type of taste.
e. Different chemicals not only excite different receptors, they also
produce different rhythms of action potentials.
3. Mechanisms of Taste Receptors

a. Saltiness receptors work by allowing salt to cross the membrane. The
higher the concentration of salt, the greater the response of the
receptors (i.e., the larger the receptor potential).
b. Sourness receptors detect acids.
c. Sweetness, bitterness, and umami receptors work by activating a G-
protein that releases a second messenger within the cell.
d. To identify the wide range of chemicals that have a bitter taste, which
are usually toxic, we have not one bitter receptor but a family of about
25 bitter receptors.
4. Taste Coding in the Brain

a. The perception of taste depends on a pattern of responses across
taste fibers.
b. Taste information from the anterior two-thirds of the tongue travels to
the brain via the chorda tympani, a branch of the seventh cranial nerve
(facial nerve). Information from the posterior tongue and throat is
carried to the brain along branches of the ninth and tenth cranial
nerves.
c. These three nerves project to the nucleus of the tractus solitarius (NTS)
in the medulla. The NTS relays information to the pons, lateral
hypothalamus, amygdala, thalamus, and two areas of the cerebral
cortex (the insula is responsible for taste, and the somatosensory
cortex is responsible for the sense of touch on the tongue).
d. Each hemisphere of the cortex receives input mostly from the
ipsilateral side of the tongue.
5. Individual Differences in Taste

a. Phenythiocarbamide (PTC) is a chemical whose taste is controlled by a
single dominant gene. Some people hardly taste PTC, others taste it
as bitter, and some taste it as extremely bitter.
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b. The prevalence of nontasters of PTC varies across cultures and is not
obviously related to spiciness of traditional cuisine in those cultures.
c. People who are insensitive to the taste of PTC are less sensitive to
other tastes as well.
d. People who taste PTC as extremely bitter are supertasters and have
the highest sensitivity to all tastes.
e. Supertasters have the largest number of fungiform papillae (the type
of papillae near the tip of the tongue).
B. Olfaction
1. Olfaction: The sense of smell; the detection and recognition of chemicals
that come in contact with membranes inside the nose.
2. Continued stimulation of an olfactory receptor produces adaptation. This
adaptation is more rapid than that of sight or hearing.
3. Olfactory Receptors
a. Olfactory cells: Neurons that line the olfactory epithelium and are
responsible for smell. In mammals, each olfactory cell has cilia
(threadlike dendrites) where receptor sites are located.
b. Olfactory receptors are made up of a family of proteins that traverse

the cell membrane seven times and respond to chemicals outside the
cell by causing changes in a G-protein inside the cell. The G-protein
provokes chemical activities that lead to an action potential.
c. It is estimated that humans have hundreds of different types of
olfactory receptor proteins. Rats and mice are believed to have a
thousand types.
3. Implication for Coding

a. In the olfaction system, the response of one receptor
can identify the approximate nature of the molecule
and the response of a larger population of receptors
enables more precise recognition. This is possible
because of the large number of olfactory receptors.
4. Messages to the Brain

a. Axons of olfactory receptors carry information to the olfactory bulb.
Each odorous chemical excites only a limited part of the olfactory
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bulb. Olfaction is coded in terms of which area of the olfactory bulb is
excited.
b. The olfactory bulb sends its axons to several parts of the cortex. The
connections are precise, as all receptors sensitive to a given group of
chemicals send information to the same small cluster of cells in the
cortex. The organization of the olfactory cortex is almost identical from
one individual to another.
c. In contrast to receptors for vision or hearing, olfactory receptors
survive for just over one month and then are replaced by new cells
that have the same odor sensitivities as the original cells.
5. Individual Differences
a. On average, women detect odors more readily than men, and the brain
responses to odors are stronger in women.
b. Young adult women exposed repeatedly to a faint odor will gradually
become more sensitive to the odor. This ability is not found in males,
girls before puberty, or women after menopause.
D. Pheromones
1. The vomeronasal organ (VNO): A set of receptors located near, but
separate from, the olfactory receptors.
2. Pheromones: Chemicals released by an animal that affect the behavior of
other members of the same species, especially sexually.
3. The receptors in the VNO are specialized to respond only to pheromones.
Each VNO receptor responds to just one pheromone and does not show
adaptation after continued exposure.
4. Unlike most mammals, the VNO is small in adult humans. Moreover, no
receptors have been found in the human VNO.
5. Humans do respond to pheromones and have at least one type of
pheromone receptor located in the olfactory mucosa.
6. Pheromones play a role in human sexual behavior similar to that in other
mammals. Pheromones can synchronize the menstrual cycles of women
who spend a lot of time together and enhance the regularity of the
menstrual cycle of a woman who is in an intimate relationship with a man.
E. Synesthesia
1. Experience of one sense in response to another sense, such as perceiving
a color when hearing a sound of a particular pitch.
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2. May be due to axons from one cortical area branching inappropriately to
adjacent cortical areas.
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CHAPTER 8: MOVEMENT
Chapter Outline
I. The Control of Movement
A. Muscles and Their Movements

1. All animal movement depends on the contractions of muscles. Vertebrate
muscles fall into three categories:
a. Smooth muscles: Control movements of the digestive system and
other internal organs.
b. Skeletal, or striated, muscles: Control movements of body in relation
to the environment.
c. Cardiac muscles: The heart muscles have properties intermediate
between those of smooth and skeletal muscles.
2. Each muscle is composed of many individual fibers and a given axon may
innervate more than one muscle fiber.
3. Neuromuscular junction: A synapse between a motor neuron axon and
muscle fiber. In skeletal muscles, acetylcholine is released at all axon
terminals at the neuromuscular junction.
4. Each muscle makes only one movement: a contraction; in the absence of
excitation it relaxes.
5. Antagonistic muscles: Are necessary for moving limbs in opposite
directions.
a. Flexor muscles allow limbs to be flexed or raised.
b. Extensor muscles extend or straighten limbs.
7. Fast and Slow Muscles
a. Even though muscle contractions are chemical processes that are
affected by temperature, fish are able to swim fast regardless of the
water temperature because they use more muscles in cold water and
fewer muscles in warmer water.
b. Fish have three kinds of muscles:
• Red muscles: Produce slow movements without fatigue.
• White muscles: Produce fast movements but fatigue quickly.
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• Pink muscles: Produce responses intermediate between the red
muscles and white muscles.
c. Humans have muscle fibers that are mixed together. Fast-twitch fibers
produce fast contractions but fatigue rapidly; slow-twitch fibers
produce less vigorous contractions without fatiguing.
d. Slow twitch fibers do not fatigue because they are aerobic—they use
oxygen during their movements.
e. Fast-twitch fibers fatigue after vigorous use, because the process is
anaerobic (reactions that do not require oxygen, although oxygen is
necessary for recovery). Anaerobic muscles produce lactate and
phosphate, which gives the sensation of muscle fatigue.
f. Humans have varying amounts of fast-twitch and slow-twitch muscle
fibers and can increase one type or the other depending on which
ones they use.
8. Muscle Control by Proprioceptors
a. Proprioceptor: A receptor that detects the position or movement of a
part of the body. Muscle proprioceptors detect the stretch and tension
of a muscle.
b. Stretch reflex: After a muscle is stretched, the spinal cord sends a
signal to contract the muscle. This reaction is caused by a stretch.
c. Muscle spindle: A kind of proprioceptor. When stretched, its sensory
nerve sends a message to a motor neuron in the spinal cord, which
sends a message back to the muscles surrounding the spindle,
causing a contraction.
d. Golgi tendon organ: Located in the tendons at opposite ends of
muscles, these proprioceptors inhibit muscle contraction when it is too
intense.
B. Units of Movement
1. Different kinds of movement depend on different kinds of control by the
nervous system.
2. Voluntary and Involuntary Movements
a. Reflexes: Consistent automatic responses to stimuli that are generally
thought to be involuntary because they are not affected by
reinforcements, punishments, and motivations e.g., a pupil
constricting to bright light.
b. Humans have very few reflexes, although infants have several not seen
in adults.
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• Grasp reflex: infant reflex where placing an object in an infant’s
hand will cause the infant to grasp the object tightly.
• Babinski reflex: infant reflex where infant will reflexively extend the
big toe and fan the others if the sole of the foot is stroked.
• Rooting Reflex: infant reflex where touching the check of an infant
will cause the infant to turn its head toward the stimulated cheek
and start to suck. This is actually not a pure reflex because its
intensity increases when the infant is hungry.
c. Infant reflexes fade away with time, as they are suppressed by axons
from the maturing brain. These reflexes sometimes reappear when the
adult brain is damaged or temporarily impaired.
d. Infants and children also have certain allied reflexes (reflexes induced
by the performance of another reflex).
e. Few behaviors can be classified as purely voluntary or involuntary
(reflexive or nonreflexive).
2. Movements Varying in Sensitivity to Feedback
a. Ballistic movements: Once initiated, this movement cannot be altered
or corrected (e.g., reflexes).
b. Completely ballistic movements are rare, as most behaviors are
subject to feedback correction.
3. Sequences of Behaviors
a. Central pattern generators: Neural mechanisms in the spinal cord or
elsewhere that generate rhythmic patterns of motor output (e.g.,
wings flapping in birds, fin movements in fish, etc.).
b. Motor programs: Fixed sequence of movements. Motor programs can
be learned or built into the central nervous system.
II. Brain Mechanisms of Movement
A. The Cerebral Cortex

1. Primary motor cortex (precentral gyrus of the frontal cortex): Stimulation of
this area elicits movements, although it is not directly connected to the
muscles.
2. Axons from the primary motor cortex go to the brainstem and spinal cord
(which have the central pattern generators to control actual muscle
movement).
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3. The cerebral cortex is particularly important for complex actions such as
writing, and less important for coughing, sneezing, gagging, laughing, or
crying.
4. Stimulation of the motor cortex can elicit complex movement patterns.
5. The motor cortex is stimulated when we imagine movement.
6. Planning a Movement
a. The primary motor cortex is important for making movement, not
planning them.
b. Posterior parietal cortex: One of the first areas to become active in
planning a movement. Keeps track of the position of the body relative
to the environment. When surgeons stimulate parts of the posterior
parietal cortex during surgery, patients report an intention to move.
c. People with damage to the posterior parietal cortex have trouble
converting their visual perceptions into actions (i.e., trouble finding
objects in space, even when describing their appearance accurately).
d. Supplementary motor cortex: Important for planning and organizing a
rapid sequence of movements (e.g., pushing, pulling, and then
turning a stick in a particular order).
e. Premotor cortex: Active during preparations for a movement and
somewhat active during the movement itself. The premotor cortex
receives information about the target in space and information about
the current position and posture of the body itself.
f. Prefrontal cortex: Responds to sensory signals that lead to
movements. Damage to this area leads to poorly planned movements.
7. Mirror Neurons
a. Neurons that are active either during preparation of a movement or
while watching someone else perform the same movement.
b. May be the basis of imitating and understanding others.
c. Experimental studies suggest that some mirror neurons are innate
while others are acquired through experience and learning.
8. Conscious Decisions and Movements
a. An interesting study showed that a readiness potential (neural activity
in the motor cortex that precedes any voluntary movement) precedes
our conscious decision to make a motor movement. This finding
suggests that voluntary decisions to make a motor movement may be
at first unconscious.
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9. Connections from the Brain to the Spinal Cord
a. Corticospinal tracts: Paths from the cerebral cortex to the spinal cord.
We have two such tracts that nearly all movements rely on.
b. Lateral corticospinal tract: Axons from the primary motor cortex and
from the red nucleus of the midbrain synapse in the spinal cord. In the
medulla lie the pyramids, where the lateral tract crosses to the
opposite (contralateral) side of the spinal cord. This tract controls
movements of the distal limbs (e.g., hands, fingers, and toes).
c. Medial corticospinal tract: Axons from the primary motor cortex, the
supplementary motor cortex, and many other parts of the cortex. This
tract also includes axons from the midbrain tectum, the reticular
formation, and the vestibular nucleus (brain area that receives input
from the vestibular system). Axons from the medial tract go to both
sides of the spinal cord and are largely responsible for neck, shoulder,
and trunk movements.
B. The Cerebellum
1. Cerebellum (Latin for “little brain”): The part of the brain most well-known
for balance and coordination. Contains more neurons than the rest of the
brain combined.
2. The most obvious effect of cerebellar damage is problems making rapid
movements that require aim and timing. For example, people with
cerebellar damage have trouble tapping a rhythm, clapping hands,
pointing at a moving object, speaking, writing, typing, or playing an
instrument. However, people with cerebellar damage are normal at
continuous activity, like drawing continuous circles. This type of activity
does not require starting or stopping an action.
3. Saccades: Ballistic eye movements from one fixation point to another.
These movements depend on impulses from the cerebellum and the
frontal cortex to the cranial nerves (patients with cerebellar damage may
have difficulty following and fixating on moving objects).
3. Finger-to-nose test: A task where a person is instructed to hold one arm
straight out and then at command to touch his or her nose as quickly as
possible. This ability relies on the cerebellar cortex to relay information to
synapses in the interior of the cerebellum. People with cerebellar damage
cannot accurately perform this task.
4. Damage to the cerebellum produces symptoms similar to alcohol
intoxication: clumsiness, slurred speech, and inaccurate eye movements.
The cerebellum is one of the first brain areas that alcohol affects.
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5. Role in Functions Other Than Movement
a. The cerebellum responds to sensory stimuli even in the absence of
movement. MRI studies show cerebellar activity when people felt
things with both hands to decide whether two objects were the same
or rubbed an object across an unmoving hand.
b. In addition to motor functions, the cerebellum appears linked to habit
formation, timing, and other psychological functions. It is also critical
for attention.
6. Cellular Organization
a. The cerebellum receives input from the spinal cord, from each of our
sensory systems via cranial nerve nuclei, and from the cerebral cortex.
The information eventually reaches the cerebellar cortex, the surface
of the cerebellum.
b. Neurons in the cerebellar cortex have the following characteristics:
• The neurons are arranged in a very precise geometrical pattern
with multiple repetitions of the same unit.
• Action potentials of parallel fibers (axons parallel to one another
but perpendicular to Purkinje cells) excite one Purkinje cell (very
flat cells in sequential planes) after another.
• Purkinje cells inhibit cells in the nuclei of the cerebellum (clusters
of cell bodies in the interior of the cerebellum) and the vestibular
nuclei in the brain stem.
• The output of Purkinje cells controls the timing of a movement,
including onset and offset.
C. The Basal Ganglia
1. The Basal Ganglia: Comprised of a group of large subcortical structures in
the forebrain (including the caudate nucleus, putamen, and the globus
pallidus).
a. The basal ganglia has multiple connections with the cerebral cortex
and the thalamus. The caudate nucleus and the putamen receive input
from the cerebral cortex. Output from the caudate nucleus and
putamen go to the globus pallidus then mainly go to the thalamus,
which relays the information to the cerebral cortex.
b. Output from the globus pallidus is constantly inhibiting the thalamus.
Input from the caudate nucleus and putamen tells the globus pallidus
to stop inhibiting the thalamus.
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c. The basal ganglia, in effect, selects which movement to make by
ceasing to inhibit it. This is particularly important for self-initiated
behaviors.
D. Brain Areas and Motor Learning
1. All the brain areas responsible for control of movement are important for
learning new skills.
2. Activity in the neurons of the motor cortex adjust their responses as a
person or animal learns a motor skill. After prolonged training, movement
patterns and activity patterns in the motor cortex become more consistent
from trial to trial.
3. The basal ganglia are critical for learning motor skills, organizing
sequences of movement into a whole, and in general for the kinds of
learning that we can’t easily express in words.
E. Inhibition of Movements
1. Antisaccade task: A task in which you are supposed to look in the opposite
direction of a moving object on the periphery of your visual field. This is
difficult because people have a strong tendency to look toward the
moving object.
2. Children aged 5-7 find the task almost impossible.
3. The ability to perform the antisaccade task develops slowly because the
prefrontal cortex is one of the slowest brain areas to reach maturity.
III. Disorders of Movement
A. Parkinson’s Disease
1. Parkinson’s disease (also called Parkinson disease): Symptoms include
rigidity, resting tremor, slow movements, and difficulty initiating physical
and mental activity. Parkinson’s disease is also associated with cognitive
deficits in memory and reasoning, as well as depression. Often the first
symptom is the loss of olfaction.
2. Parkinson’s Disease strikes 1–2% of people over the age of 65.
3. Causes
a. The immediate cause of PD is the gradual progressive death of
neurons, especially in the substantia nigra.
b. A loss of dopamine activity in the substantia nigra leads to less
stimulation of the motor cortex and slower onset of movements.
c. The average person over 45 loses substantia nigra neurons at a rate of
1% per year. Most people have enough to spare, but when the
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surviving number of substantia nigra neurons declines below 20-30%
of normal, Parkinsonian symptoms begin.
d. Research suggests that genetics may be important for early-onset
Parkinson’s disease, but not for the more common form of Parkinson’s
that begins later in life.
e. MPTP: A chemical that our bodies convert to MPP+, which is a toxin
that destroys dopamine neurons. Illegal drugs contaminated with
MPTP can induce Parkinson’s disease-like symptoms.
f. Cigarette smoking and coffee drinking decrease the chances of
developing Parkinson’s Disease. Chemical in these substances (other
than nicotine and caffeine—since decaffeinated coffee and nicotine
free cigarettes work just as well) reduce the risks of damage to the
mitochondria.
g. Parkinson’s disease probably results from a mixture of causes.
Damage to the mitochondria may be a common factor in all the
different causes of Parkinson’s disease.
5. L-Dopa Treatment
a. L-Dopa: A precursor to dopamine. Commonly used as a treatment for
Parkinson’s disease.
b. L-Dopa treatment is disappointing in several ways:
• Effectiveness varies, with some patients receiving no benefit from
this treatment, and its effectiveness is limited to the early and
intermediate stages of disease.
• It does not prevent the continued loss of dopamine-containing
neurons and it may contribute to the death of neurons.
• It produces harmful side effects, especially in patients with the
most severe symptoms.
6. Other Therapies
a. Because of the limitations of L-Dopa therapy, the following alternatives
have been developed:
• Antioxidant drugs
• Direct dopamine agonists
• Glutamate or adenosine antagonists
• Drugs that block a calcium channel that occurs more commonly in
old age
• Drugs that stimulate cannabinoid receptors
• Gene therapy
• Neurotrophins
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• Apoptosis blockers
• High-frequency electrical stimulation of the globus pallidus or
subthalamic nucleus
b. Research in partial brain transplants is also ongoing. Early studies in
humans with transplanted adrenal and fetal cells suggested that this
treatment was not very beneficial to patients. Additional animal
research indicates that improved strategies using neurotrophins and
stem cells (immature cells that are capable of differentiating into a
wide variety of other cell types, depending on where they are in the
body) are beginning to show promise.
B. Huntington’s Disease
1. Huntington’s Disease (also called Huntington’s chorea or Huntington
disease): Severe neurological disorder with symptoms that include
twitches, tremors, and writhing movements. Huntington’s disease strikes
one person in 10,000.
2. Huntington’s disease is associated with gradual, extensive brain damage,
which is especially severe in the caudate nucleus, putamen, and globus
pallidus, but also occurs in the cerebral cortex.
3. Psychological symptoms include depression, memory deficits, anxiety,
hallucinations, delusions, poor judgment, alcoholism, drug abuse, and
sexual disorders. Sometimes the psychological symptoms precede the
motor disorders.
4. Huntington’s disease onset can occur at any age, but most often appears
between the ages of 30 and 50. The earlier the onset, the more rapid the
deterioration.
5. Heredity and Presymptomatic Testing
a. Huntington’s disease is caused by an autosomal dominant gene on
chromosome 4. The gene can be identified by a presymptomatic test
(before the onset of symptoms) with almost 100% accuracy.
b. The critical region of the gene includes a sequence of bases C-A-G
which is repeated 11 to 24 times in most people. People with up to 35
C-A-G repeats are safe from Huntington’s disease, people with 36-38
might get it, and people with 39 or more are likely to get the disease.
c. The gene for Huntington’s disease codes for the protein huntingtin,
which is found throughout the human body. In the brain, huntingtin is
found within neurons and not on their membranes.
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d. The abnormal form of huntingtin interferes with several metabolic
pathways and its discovery may make it possible to develop a
treatment for Huntington’s disease.
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CHAPTER 9: WAKEFULNESS AND SLEEP

Chapter Outline
I. Rhythms of Wakefulness and Sleep
A. Endogenous Cycles
1. Endogenous circannual rhythm: An internal calendar that prepares a
species for annual seasonal changes.
2. Endogenous circadian rhythm: Internal rhythms that last about a day (e.g.,
wakefulness and sleepiness).
3. In humans, the circadian rhythm has a self-generated duration of about 24
hours.
4. Circadian rhythms are also present in eating, drinking, urination, secretion
of hormone, sensitivity to drugs, and other variables. Body temperature
also fluctuates (36.7 degrees Celsius at night and 37.2 in the late
afternoon).
5. Circadian rhythms also affect mood. On average, teenagers showed
increase in positive mood from waking until late afternoon, then a slight
decline from then to bedtime. Most people report their most pleasant
mood around 5pm and their least pleasant mood around 5am.
6. One’s natural circadian rhythm predisposes them to be either “larks” (early
risers) or “owls” (evening people). This rhythm may change with age.
B. Setting and Resetting the Biological Clock

1. Zeitgeber: Stimulus that is necessary for resetting the circadian rhythm.
Light is the dominant zeitgeber for land animals.
2. Astronauts exposed to 45-minute intervals of light and dark are never fully
alert during their wakeful periods and they sleep poorly during their rest
periods.
3. Most people are ill-rested and inefficient for days after the shift to daylight
savings time.
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4. Blind people sometimes use other zeitbegers (noise, temperature, meals,
etc.) but those not sensitive enough to secondary zeitbegers often
experience insomnia at night and sleepiness during the day.
C. Jet Lag
a. Jet lag: A disruption of our biological rhythms due to crossing time
zones.
b. Phase-delay: What happens to our circadian rhythms when we travel
west, as we stay awake late and awaken the next day already partly
adjusted to the new schedule.
c. Phase-advance: What happens to our circadian rhythms when we
travel east, as we tend to sleep and awaken earlier than usual.
d. Recent studies have indicated that repeated adjustments of the
circadian rhythm can increase levels of cortisol, which can damage the
hippocampus and cause memory loss.
D. Shift Work
a. Night shift workers often have difficulty adjusting to their wake/sleep
cycle (e.g., waking up groggy, not sleeping well during the day, etc.).
Working under lights comparable to noonday may help shift the
circadian rhythms.
b. Even after years of a night shift schedule, workers continue to feel
groggy on the job and sleep poorly during the day. Their body
temperature continues to peak when they are sleeping in the day
instead of while they are working at night.
E. Mechanisms of the Biological Clock

1. The Suprachiasmatic Nucleus (SCN)
a. Nucleus located above the optic chiasm in the hypothalamus. The
SCN controls the rhythms for sleep and temperature. The neurons of
the SCN generate impulses that follow a circadian rhythm.
b. There is a genetic mutation in hamsters that causes the SCN to
generate a 20-hour circadian rhythm. When the SCN of these
hamsters with a 20-hour rhythm was transplanted into adult hamsters,
the adults produced a 20-hour rhythm.
2. How Light Resets the SCN
a. The SCN is reset by the retinohypothalamic path that extends directly
from the retina to the SCN.
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b. The retinal ganglion cells that reset the SCN are different from the
ganglion cells that contribute to vision and have their own
photopigment called melanopsin that responds to slow changes in
overall duration of light.
c. These special ganglion cells are located near the nose, not evenly
throughout the retina. This way blind people have enough input to
the melanopsin-containing ganglion cells to entrain their waking and
sleeping cycle to the local pattern of sunlight.
3. The Biochemistry of the Circadian Rhythm

a. In flies, the SCN regulates the circadian rhythms through the
regulation of two genes, period (per) and timeless (tim). The per and
tim genes code for the proteins PER and TIM, respectively. Early in the
morning, the concentration of both PER and TIM are low and they
increase during the day. In the evening, protein concentrations are
high and result in sleepiness. During the night, the genes stop
producing the proteins.
b. When PER and TIM levels are high, they feed back to inhibit the genes
that produce the messenger RNA molecules. When levels are low, the
result is wakefulness.
c. Analyzing the mechanism in flies lead to research on humans.
Mammals have three versions of PER and several versions of TIM.
d. In humans, mutations in genes producing PER cause alterations in
sleep schedules.
4. Melatonin
a. SCN regulates waking and sleeping by controlling the pineal gland
which releases the hormone melatonin, which increases sleepiness.
Melatonin release usually starts 2 or 3 hours before bedtime.
b. Melatonin stimulates receptors in the SCN to reset the biological
clock.
II. Stages of Sleep and Brain Mechanisms
A. Sleep and Other Interruptions of Consciousness

1. Sleep: A state that the brain actively produces, characterized by decreased
response to stimuli.
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2. Coma: An extended period of unconsciousness caused by head trauma,
stroke, or disease. Characterized by low brain activity throughout the day
and little or no response to stimuli, including pain.
3. Vegetative State: A person alternates between periods of sleep and
moderate arousal, although they show no awareness of their
surroundings.
4. Minimally Conscious State: A person shows occasional, brief periods of
purposeful actions and limited speech comprehension.
5. Brain Death: No sign of brain activity and no response to stimulation. In
this case, physicians generally wait 24 hours before pronouncing death.
B. Stages of Sleep
1. The electroencephalograph (EEG) records gross electrical potentials in an
area of the brain through electrodes attached to the scalp.
2. Polysomnograph: A combination of EEG and eye-movement records.
3. Alpha waves have a frequency of about 8-12 brain waves per second;
these waves are typical of a relaxed state of consciousness.
4. Stage 1 sleep is a stage of light sleep noted by the presence of irregular,
jagged, low-voltage waves.
5. Stage 2 sleep is characterized by sleep spindles (a burst of 12-14 Hz waves
that last approximately 0.5 second) and K-complexes (sharp, high-
amplitude waves followed by a smaller, positive wave).
6. Stages 3 and 4 are known as slow-wave sleep (SWS), which is comprised
of slow, large-amplitude waves.
C. Paradoxical or REM Sleep

1. Paradoxical sleep: Sleep stage discovered in cats in which the brain is very
active but muscles are completely relaxed. Named “paradoxical” because
it is deep sleep in some ways and light in others.
2. Rapid eye movement (REM) sleep: Same as paradoxical sleep.
Researchers discovered that repeated eye movements were associated
with paradoxical sleep. Also characterized by fast low-voltage brain
waves, plus breathing and heart rates similar to stage 1 sleep. Paradoxical
sleep is synonymous with REM sleep, except that many animal species lack
eye movements.
3. Non-REM (NREM) sleep: The stages of sleep other than REM.
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4. When people fall asleep, they enter stage 1, followed by stages 2, 3, and
4, in that order. Then they cycle back from stage 4 through stages 3, 2,
and then enter rapid eye movement (REM) sleep.
5. After entering REM sleep, the sleep cycle sequence repeats, with each
complete cycle lasting 90 minutes.
6. Early in the night, stages 3 and 4 predominate, but toward morning, stage
4 grows shorter and REM grows longer.
7. REM sleep is associated with dreaming, but dreams can happen in non-
REM sleep.
D. Brain Mechanisms of Arousal and Attention

1. Brain Structures of Arousal and Attention
a. Reticular formation: A structure that extends from the medulla into the
forebrain. Lesions through the reticular formation decrease arousal.
b. Pontomesencephalon: A part of the reticular formation that
contributes to cortical arousal. Stimulation of the
pontomesencephalon awakens a sleeping individual or increases
alertness in someone already awake.
c. A structure in the pons that is inactive at most times but emits
impulses, releasing norepinephrine, in response to meaningful events.
The locus coeruleus is also important for storing information. The
locus coeruleus is usually silent during sleep.
d. Certain areas of the hypothalamus stimulate arousal by releasing the
neurotransmitter histamine, which produces excitatory effects
throughout the brain. Antihistamine drugs produce drowsiness if they
cross the blood-brain barrier.
e. Locus coeruleus A different group of axons from the hypothalamus
(primarily the lateral nucleus of the hypothalamus) release the peptide
neurotransmitter orexin (also called hypocretin). Orexin is necessary
for staying awake.
f. Basal forebrain: An area just anterior and dorsal to the hypothalamus.
Some of the axons from the basal forebrain release GABA and are
essential for sleep. These neurons receive input from the anterior and
preoptic areas of the hypothalamus. Another set of axons in the basal
forebrain release acetylcholine.
2. Sleep and the Inhibition of Brain Activity

a. During sleep, body temperature and metabolic rate decrease slightly.
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b. Sleep depends on GABA-mediated inhibition. While spontaneously
active neurons continue to fire at a normal rate, we are unconscious
because GABA inhibits synaptic activity.
c. Sleep can be localized. Sleepwalking is possible because a
sleepwalker is awake in one part of the brain and asleep in another
part.
E. Brain Function in REM Sleep

1. During REM sleep, activity increases in the pons, the limbic system, and
the parietal and temporal cortex of the brain. Activity decreases in the
primary visual cortex, the motor cortex, and the dorsolateral prefrontal
cortex.
2. PGO (pons-geniculate-occipital) waves: A distinctive pattern of high-
amplitude electrical potentials associated with REM sleep. The waves are
detected first in the pons, shortly afterward in the lateral geniculate
nucleus of the thalamus, and then in the occipital cortex.
3. REM sleep depends on both serotonin and acetylcholine activity for its
onset and continuation. Stimulation of acetylcholine synapses quickly
moves a sleeper into REM, and serotonin interrupts or shortens REM
sleep. Norepinephrine from the locus coeruleus also blocks REM sleep.
F. Sleep Disorders
1. Insomnia: Inadequate sleep characterized by how one feels the following
day.
2. Insomnia can result from a number of causes, including noise,
uncomfortable temperatures, stress, pain, diet, and medications. Certain
psychiatric and neurological disorders (e.g., epilepsy, Parkinson’s disease,
brain tumors, depression, and anxiety) are also associated with insomnia.
3. Insomnia may be due to shifts in circadian rhythms (e.g., trying to sleep
while body temperature rises).
a. Phase delayed: shift in rhythm where someone has trouble falling
asleep at the usual time.
b. Phase advanced: shift in rhythm where someone falls asleep easily but
awakens early.
4. Paradoxically, the use of tranquilizers, such as sleeping pills, can lead to
insomnia.
5. Sleep Apnea
a. Inability to breathe during sleep.
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b. Symptoms include sleepiness during the day, impaired attention,
depression, and sometime heart problems.
c. People with sleep apnea have many brain areas that appear to have
lost neurons. They consequently show deficiencies of learning,
reasoning, attention, and impulse control.
d. Research with mice suggests that sleep apnea leads to the
aforementioned deficiencies (not the other way around) because of
the deprivation of oxygen.
e. Genetics, hormones, and obesity are all causes of this disorder.
6. Narcolepsy
a. A disorder characterized by frequent unexpected periods of
sleepiness during the day.
b. Symptoms include gradual or sudden attacks of sleepiness, occasional
cataplexy (attack of muscle weakness while awake), sleep paralysis
(inability to move while asleep), and hypnagogic hallucination
(dreamlike experiences occurring at the onset of sleep).
c. Each of the symptoms of narcolepsy is interpreted as REM sleep
intruding into wakefulness.
d. People with narcolepsy lack the hypothalamic cells that produce and
release orexin.
e. Narcolepsy is currently treated with stimulant drugs such as
methylphenidate (Ritalin).
7. Periodic limb movement disorder: Repeated involuntary movements of
the legs and arms that can cause insomnia. The limb movements occur
mostly during NREM sleep. This disorder is often treated with tranquilizers.
8. REM behavior disorder: Disorder where people move around vigorously
during their REM periods apparently acting out their dreams. Likely due to
the inability of the pons to inhibit spinal motor neurons.
9. Night Terrors and Sleepwalking
a. Night terrors: An abrupt, anxious awakening from NREM sleep; this
disorder is more common in children than adults.
b. Sleepwalking: Usually occurs during stages 3 or 4 early in the night
and is more common in children than adults. Usually runs in families.
It is more common when people are sleep deprived or under unusual
stress.
c. Sleep sex or “Sexsomnia”: an analogous condition in which sleeping
people engage in sexual behavior either with a partner or by
masturbation.
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III. Why Sleep? Why REM? Why Dreams?
A. Functions of Sleep
1. Sleep and Energy Conservation
a. Sleep may have evolved to serve different purposes that it did in the
distant past.
b. For most animals, sleep conserves energy during times when the
animal is inefficient. Animals also increase sleep during food
shortages (i.e., hibernation).
c. Animal species vary in their sleep habits in accordance with how many
hours per day they devote to finding food, how safe they are from
predators while they sleep, and other aspects of their way of life.
d. Some species that are efficient at all hours of the day and night have
evolved to never sleep (e.g., some fish species, dolphins after giving
birth, some bird species).
2. Sleep and Memory
a. Another function of sleep is improved memory. Young adults
deprived of a night’s sleep show deficits on memory tasks. In contrast,
if someone learns something and then goes to sleep, even for a short
time, memory after sleeping is improved.
b. Research shows that the patterns that occur in the brain during sleep
resembled those that occurred during learning, yet were more rapid
during sleep. This suggests the brain replays its daily experiences
during sleep and reinforces the learning through repetition.
c. Sleep strengthen memory selectively by reinforcing certain synaptic
connections and weakening others to prevent over-activity of the
brain.
d. During sleep, the brain also exhibits spindle activities of sleep
spindles, which increase in number after new learning.
3. Functions of REM Sleep
a. Species with the most total sleep also have the highest percentage of
REM sleep. Human infants spend more time in REM sleep and get
more total sleep than adults. Adults who get the most sleep have the
most REM sleep and adults who get the least sleep get the least
amount of REM.
b. Depriving people of sleep early in the night (non-REM sleep) leads to
impairment of verbal learning. Depriving people of sleep the latter
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half of the night (REM sleep deprivation) leads to impaired
consolidation of learned motor skills. REM deprivation also leads to
increased attempts at REM sleep.
c. REM sleep has been implicated as a useful tool for memory storage. It
is a way of consolidating different types of memories.
d. Research suggests that REM sleep may also be a way of getting
oxygen to the corneas.
C. Biological Perspectives on Dreaming

1. Activation-Synthesis Hypothesis: During sleep, many brain regions
become activated, so the brain creates a story to make sense of all this
activity.
4. Clinico-Anatomical Hypothesis: Either internal or external stimulation
activates parts of the parietal, occipital, and temporal cortex. No visual
information overrides the stimulation and no criticism of the prefrontal
cortex censors it, so it develops into hallucinatory perceptions.
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CHAPTER 10: INTERNAL REGULATION

Chapter Outline
I. Temperature Regulation
1. Several species of animals have developed behaviors designed to regulate

body temperature.
a. A small male garter snake produces female pheromones and attract
larger males, who, in the process of trying to copulate with the smaller
male, warm him.
b. Some bird species that stand on one leg do so in cold weather so that
the other leg is warmed under their body.
c. Vultures sometimes defecate on their legs on hot days so that the
evaporation process cools them.
d. Toucans have huge bills so that they can direct blood flow to the bill and
either cool or warm themselves accordingly.
e. Lizards huddle to protect themselves against rapidly changing
temperatures.
2. Homeostasis and Allostasis

a. Homeostasis: Temperature regulation and other biological processes
that keep certain body variables within a fixed range.
b. Set point: Level at which a homeostatic process maintains a variable.
c. Negative feedback: Processes that reduce discrepancies from the set
point.
d. Allostasis: Dynamic and adaptive changes in the body’s set points in
response to changes in its life or changes in the environment.
3. Controlling Body Temperature

a. Temperature regulation is a high biological priority.
b. Basal Metabolism: Energy used to maintain a constant body temperature
at rest. Twice as much energy is used for temperature regulation as all
other activities combined.
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c. Poikilothermic: Animals with body temperatures the same as their
environment (i.e., fish and lizards).
d. Homeothermic: Animals with physiological mechanisms that maintain an
almost constant body temperature despite variations in environmental
temperature. These types of animals generate heat in proportion to their
total mass but radiate heat in proportion to their surface area. For these
animals, sweating, licking themselves, and panting are used as cooling
mechanisms. Shivering and fluffing are used as heating mechanisms.
e. The Advantages of Constant High Body Temperature
• Mammals maintain a body temperature of 37°C because maintaining
a high body temperature keeps the animal ready for rapid movement
even in cold temperatures.
• Mammals may have developed even higher body temperatures
except that proteins become unstable at temperatures above 40°C.
• Reproductive cells require a somewhat cooler temperature than other
body cells.
f. Brain Mechanisms
• The brain regions most critical for temperature control are the
anterior hypothalamus and the preoptic area of the hypothalamus
(preoptic because it is near the optic chiasm). Because of the close
relationship between these areas, they are often treated as one area,
the preoptic area/anterior hypothalamus (POA/AH).
• The POA/AH monitors body temperature by monitoring its own
temperature and by receiving input from temperature-sensitive skin
and spinal cord receptors.
g. Fever
• Infection of the body by bacteria or viruses causes fever. The fever is
not a part of the illness; it is instead a part of the body’s defenses.
Once infected, the body mobilizes its leukocytes (white blood cells) to
attack these foreign substances. Leukocytes release small proteins
called cytokines, which attack the intruders and communicate with the
brain.
• A fever represents an increased set point for body temperature.
Moving to a cooler room will not lower a fever; it will just cause the
body to work harder to maintain its temperature.
• Newborn rabbits, whose hypothalamus is immature, prefer a room
warm enough to increase their body temperature in response to an
infection. In other words, they develop a fever by behavioral means.
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• Fever works because certain types of bacteria grow less vigorously at
high temperatures, and it enhances the activity of the immune system.
However, a fever above 39°C does more harm than good, and a fever
above 41°C is life threatening.
II. Thirst
A. Mechanisms of Water Regulation

B. Different species have different strategies for maintaining water. Humans, like
beavers, drink more than is needed and excrete the rest.
C. For humans, when your body needs water, the posterior pituitary gland
releases vasopressin, also known as antidiuretic hormone (ADH), which
enables the kidneys to reabsorb water and secrete highly concentrated urine.
D. Osmotic Thirst
1. Thirst can be divided into two types: thirst due to eating salty foods
(osmotic thirst) and thirst due to a loss of fluids (hypovolemic thirst).
2. Osmotic pressure: The tendency of water to flow across a semipermeable
membrane from an area of low concentration to areas of high
concentration. In cells, the membrane works as a semipermeable
membrane and water, but not all solutes, flows freely between the
extracellular fluid (fluid outside the cell) and intracellular fluid (fluid inside
the cell).
3. Osmotic thirst: Occurs when certain neurons detect their own loss of
water. This loss of water happens when solute concentrations in the
extracellular fluid are higher than the concentration of solutes in the
intracellular fluid, causing water to be drawn from the intracellular
compartment to dilute the solutes in the extracellular fluid.
4. Organum Vasculosum Laminae Terminalis (OVLT) and subfornical organ:
Areas located around the third ventricle that are responsible for detecting
osmotic pressure.
5. The brain also receives information from receptors in the periphery,
including the stomach, that detect high levels of sodium.
6. The supraoptic nucleus and paraventricular nucleus are brain areas
located in the hypothalamus that control the rate at which the posterior
pituitary gland releases vasopressin. Both of these brain areas and the
lateral preoptic area (which controls drinking) receive information from the
OVLT, the subfornical organ, the stomach, and elsewhere.
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7. Mechanisms exist that prevent too much water consumption. The body
monitors swallowing and detects the water contents of the stomach and
intestines. Those messages suppress thirst long before the ingested water
can reach the brain.
E. Hypovolemic Thirst and Sodium-Specific Hunger
1. When you lose a significant amount of body fluid by bleeding, diarrhea, or
sweating, the body will release hormones, including vasopressin and
angiotensin II, that constrict blood vessels. When blood volume decreases,
kidneys release the hormone rennin, which splits a portion off
angiotensinogen (a large protein in the blood) to form angiotensin I,
which is then converted into angiotensin II; this hormone constricts blood
vessels in order to reverse the loss of blood volume.
2. Angiotensin II triggers hypovolemic thirst (thirst based on low volume).
During hypovolemic thirst the body needs to replenish both water and lost
solutes such as salt.
3. Whereas an animal with osmotic thirst needs water, one with hypovolemic
thirst can’t drink much pure water because it would dilute its body fluids.
4. Specific sodium cravings (due to bleeding or excessive sweating) are
caused by the release of aldosterone, a hormone which causes the
kidneys, salivary glands, and sweat glands to conserve sodium and excrete
more watery fluids than usual. Aldosterone and angiotensin II together
change the properties of the neurons in the nucleus of the tractus
solitarius (part of the taste system) such that they begin reacting to salt in
nearly the same way they would to sugar.
III. Hunger
A. Digestion and Food Selection

1. Digestion begins in the mouth, where food is broken down by enzymes in
the saliva. Food then travels down the esophagus to the stomach, where
hydrochloric acid and enzymes digest proteins. A round sphincter muscle
(located between the stomach and the intestines) allows food to
periodically enter the intestines. Food then enters the small intestine,
which is the main site for nutrient absorption into the bloodstream.
These digested nutrients are carried by the blood to cells throughout the
body, which use some of the nutrients and store the rest as excess. The
large intestine absorbs water and minerals and lubricates remaining
materials for excretion.
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2. Consumption of Dairy Products
a. Newborn mammals survive on mother’s milk and then eventually stop
nursing.
b. Many mammals lose the intestinal enzyme lactase, which allows them
to metabolize lactose (sugar found in milk). Losing the enzyme lactase
may be an evolved mechanism to encourage weaning.
c. Milk consumption then causes stomach cramps and gas.
d. The ability to consume large amounts of milk products varies
geographically. In China and surrounding countries, nearly everyone
lacks the ability to metabolize lactose.
3. Food Selection and Behavior

a. Many unsubstantiated myths exist about food selection and behavior,
including the idea that turkey makes you sleepy because of its
tryptophan content and sugar makes kids hyperactive.
b. The belief that fish is brain food has support. Recent studies suggest
that fish contain oils that are helpful for brain functioning, including
memory and reasoning abilities.
B. Short- and Long-term Regulation of Feeding

1. The brain gets messages from the mouth, stomach, intestines, fat cells,
and elsewhere to regulate eating.
2. Oral Factors
a. Tasting and chewing food is an important part of eating. Participants
in a study where liquid food was pumped in their stomachs found the
meals unsatisfying and reported a desire to taste or chew something.
b. In sham-feeding experiments, everything an animal eats leaks out a
tube connected to the esophagus or stomach (under these
conditions, animals consume several times as much as untreated
animals during each meal).
c. These studies demonstrate that although taste and mouth are
important cues, they are not sufficient alone to produce satiety.
3. Stomach and Intestines
a. Usually, we end a meal before the food reaches the blood. Satiety
signals are therefore based on other aspects of eating such as
stomach distension.
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b. Studies show that stomach distention is sufficient to produce satiety,
though not necessary because those with stomachs surgically
removed still report satiety.
c. The vagus nerve (cranial nerve X) carries information to the brain
regarding the stretching of stomach walls, providing a major basis for
satiety.
d. The splanchnic nerves convey information about the nutrient contents
of the stomach, carrying impulses back and forth from the spinal cord
to the digestive organs.
e. The duodenum is part of the small intestine adjoining the stomach.
The duodenum also releases a hormone called oleoylethanolamide
(OEA) to cause satiety.
f. Cholecystokinin (CCK): A hormone released by the duodenum to
inhibit appetite.
4. Glucose, Insulin, and Glucagon
b. Insulin: Facilitates entry of glucose from the bloodstream into the
body's cells. (Brain cells do not need insulin for glucose to enter).
c. Glucagon: Stimulates the liver to convert stored glycogen to glucose.
d. After a meal, insulin levels rise, glucose readily enters the cell, and
appetite decreases. As time passes, blood glucose levels fall, the body
causes an increase in glucagon release, and hunger is induced.
e. Chronically high insulin levels cause increased eating because blood
glucose levels are low. In autumn, animals getting ready for
hibernation experience rapid weight gain because of high insulin
levels. Humans also eat more in autumn that in other seasons.
f. Diabetics eat more food than usual but excrete much of their glucose
and lose weight due to poor insulin blood levels.
5. Leptin
a. A recently discovered hormone that monitors the body’s fat reserves
to account for day-to-day mistakes in consumption.
b. Leptin is normally made by fat cells so that the fatter cells, the higher
the levels of leptin. When fat cell reserves are low, there are low levels
of leptin and hunger increases.
c. Each meal also releases leptin, as a short-term monitor about the
body’s fat reserves.
d. Some mice genetically predisposed to obesity fail to produce leptin.
The brain then acts as if the body has no fat stores and signals the
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mouse to eat more and be less active (to conserve energy). Leptin
injections have reversed these symptoms in mice.
e. Humans become less sensitive to leptin during pregnancy. Obesity
also lowers leptin sensitivity by damaging the endoplasmic reticulum
in neurons of the hypothalamus. This can only be reversed through
physical exercise.
C. Brain Mechanisms
1. The Arcuate Nucleus and Paraventricular Hypothalamus

a. The arcuate nucleus of the hypothalamus has a set of neurons
sensitive to hunger signals and another set of cells sensitive to satiety
signals. The hunger-sensitive cells receive input from the taste
pathway and from ghrelin (a neurotransmitter released from the
stomach during periods of food deprivation), released by axons.
b. The satiety-sensitive cells receive input for both short-and long-term
satiety. Input includes CCK release from the intestines, and insulin
release from both blood glucose and body fat. Leptin also provides
input to the arcuate nucleus.
c. Much of the input from the arcuate nucleus goes to the paraventricular
nucleus (PVN). The PVN inhibits the lateral hypothalamus (an area
important for eating) and is involved in satiety. If the PVN is damaged,
rats eat larger than normal meals.
d. α-Melanocyte stimulating hormone is released from the satiety-
sensitive cells of the arcuate nucleus to the PVN. Deficiencies in
melanocortin receptors cause people to overeat as they do not
respond to satiety signals.
e. Inhibitory transmitters from the hunger-sensitive cells of the arcuate
nucleus including GABA, neuropeptide Y (NPY), and agouti-related
peptide (AgRP) inhibit the PVN and the satiety-sensitive cells of the
arcuate nucleus.
f. NPY cells also have a pathway to the orexin-producing cells of the
lateral hypothalamus. Orexin stimulates activity and the onset of meals
but has a minor overall effect on feeding behavior.
2. The Lateral Hypothalamus
a. The lateral hypothalamus controls insulin secretion, alters taste
responsiveness, and facilitates feeding in other ways. Damage to the
lateral hypothalamus causes an animal to refuse food and water.
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b. Contributions of the lateral hypothalamus include: altering the taste of
food (when one is hungry, food tastes better), causing cortical cells to
increase their response to taste, smell, or sight of food, controlling
insulin secretion, controlling digestive secretions.
3. Medial Areas of the hypothalamus
a. Ventromedial hypothalamus (VHM): Damage centered around this
area leads to overeating and weight gain (after gaining weight, these
animals become picky eaters, as they consume bitter foods far less
than normal but eat more than normal of a sweetened or normal diet).
However, this effect, known as the ventromedial hypothalamic
syndrome, usually requires the lesion to extend outside the
ventromedial nucleus and invade nearby axons.
D. Eating Disorders
1. Obesity and anorexia exist on different sides of the spectrum of eating
disorders.
2. Research shows that when given the option of a “buffet” of high-calorie
foods, rats are unable to pass up the options. Soon they become obese
and lose interest in rewards other than food. Humans show the same
tendency.
3. Recent research shows that there is little correlation between obesity and
mood. This goes against the notion that obesity is caused by
psychological issues such as depression.
4. Exposure to a high-fat diet before birth predisposes the offspring to
increased appetite and body weight.
5. Genetics and Body Weight
a. A Danish study showed that the weights of adopted children
correlated better with their biological parent than their adopted
family. This could be evidence for either a genetic or prenatal
environmental contribution to weight.
b. Specific genes have been linked with obesity. A mutated gene for
melanocortin can cause obesity.
c. Syndromal obesity: obesity that results from a medical condition. The
genetic disorder Prader-Willi syndrome leads to obesity, possibly by
inducing high levels of the peptide ghrelin.
d. Most cases of obesity result from the combined influences of genes
and the environment.
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6. Weight Loss
a. Obesity is now classified as a disease in the United States.
b. Dieting alone is rarely effective when done alone. This is because most
obese people will fail to sustain the diet. Psychologists now suggest
implementing small changes.
c. Changing lifestyle including increasing exercise and decreasing eating
is most effective. This combination helped 20-40% of people keep
weight off for at least two years.
d. Non-diet soft drinks contain fructose, a sugar that does not stimulate
normal satiety pathways. Diet soft drinks contain artificial sugars that
cause the body to unlearn the association between the taste of
“sweet” and calories.
e. Appetite suppressants such as sibutramine (Meridia), and drugs that
block fat absorption such as orlistat (Xenical) can be effective.
f. Gastric bypass surgery removes part of the stomach so that smaller
meals produce satiety.
7. Bulimia Nervosa
a. Condition in which people alternate between dieting and overeating.
b. Some individuals with this disorder force vomiting after meals.
c. Most bulimics suffer from depression, anxiety, or other emotional
problems.
d. People with bulimia have lower than normal levels of CCK, increased
release of ghrelin, and alterations in several other hormones and
transmitters that regulate eating. These changes are likely a product to
bulimia and not the cause. After therapy, the ghrelin and other body
chemicals return toward normal levels.
e. Bulimia shares many similarities with drug addiction. Eating tasty
foods activate the same brain areas as addictive drugs, such as the
nucleus accumbens.
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Jose Rizal University

College of Liberal Arts, Criminology and Education

A. General Principles of Perception

B. The Eye and Its Connections to the Brain

College of Liberal Arts, Criminology and Education

C. Visual Receptors: Rods and Cones

College of Liberal Arts, Criminology and Education

College of Liberal Arts, Criminology and Education

E. An Overview of the Mammalian Visual System

F. The Neural Basis of Visual Perception

G. Processing in the Retina

College of Liberal Arts, Criminology and Education

H. The Primary Visual Cortex

College of Liberal Arts, Criminology and Education

I. Development of the Visual Cortex

College of Liberal Arts, Criminology and Education

J. The “What” and “Where” Paths

College of Liberal Arts, Criminology and Education

K. Detailed Analysis of Shape

College of Liberal Arts, Criminology and Education

College of Liberal Arts, Criminology and Education

CHAPTER 7: OTHER SENSORY SYSTEMS

A. Sound and the Ear

2. Structures of the Ear

College of Liberal Arts, Criminology and Education

College of Liberal Arts, Criminology and Education

C. The Auditory Cortex

College of Liberal Arts, Criminology and Education

II. The Mechanical Senses

College of Liberal Arts, Criminology and Education

College of Liberal Arts, Criminology and Education

3. Ways of Relieving Pain

College of Liberal Arts, Criminology and Education

College of Liberal Arts, Criminology and Education

III. The Chemical Senses

2. How Many Kinds of Taste Receptors?

College of Liberal Arts, Criminology and Education

3. Mechanisms of Taste Receptors

4. Taste Coding in the Brain

5. Individual Differences in Taste

College of Liberal Arts, Criminology and Education

b. Olfactory receptors are made up of a family of proteins that traverse

3. Implication for Coding

4. Messages to the Brain

College of Liberal Arts, Criminology and Education

College of Liberal Arts, Criminology and Education

College of Liberal Arts, Criminology and Education

I. The Control of Movement

A. Muscles and Their Movements

College of Liberal Arts, Criminology and Education

College of Liberal Arts, Criminology and Education

II. Brain Mechanisms of Movement

A. The Cerebral Cortex

College of Liberal Arts, Criminology and Education

College of Liberal Arts, Criminology and Education

College of Liberal Arts, Criminology and Education

College of Liberal Arts, Criminology and Education

III. Disorders of Movement

College of Liberal Arts, Criminology and Education

College of Liberal Arts, Criminology and Education

College of Liberal Arts, Criminology and Education

College of Liberal Arts, Criminology and Education