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PYC4813 – Cognitive Neuroscience Exam Preparation Summaries Chapters 5 – 14 Learning Objectives Questions and Answers $11.24   Add to cart

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PYC4813 – Cognitive Neuroscience Exam Preparation Summaries Chapters 5 – 14 Learning Objectives Questions and Answers

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PYC4813 – Cognitive Neuroscience Exam Preparation Summaries Includes: Chapters 5 – 14 Learning Objectives Questions and Answers Taken from the prescribed book: Kalat, J.W. (2016). Biological psychology (12th ed.). London: Cengage Learning

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  • April 27, 2024
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PYC4813 – Cognitive Neuroscience Exam Preparation Summaries



Includes: Chapters 5 – 14 Learning Objectives Questions and Answers


Taken from the prescribed book: Kalat, J.W. (2016). Biological psychology
(12th ed.). London: Cengage Learning




Compiled by: PsychHonours Student

,PYC4813 CHAPTER HEADINGS

Chapter 5: Vision

Chapter 6: Other sensory Systems

Chapter 7: Movement

Chapter 8: Wakefulness and sleep

Chapter 9: Temperature Regulation

Chapter 11: Emotional Behaviours

Chapter 12: The biology of learning and memory

Chapter 13: Cognitive functions

Chapter 14: Psychological disorders


Chapter 10 wasn’t included in the syllabus

,CHAPTER 5: VISION

1 Remember that we see because light strikes the retina, sending a message to
the brain

THE EYE AND ITS CONNECTIONS TO THE BRAIN

Light enters the eye through an opening in the centre of the iris called the “pupil.” It is
focused by the lens (adjustable) and cornea (not adjustable) and projected onto the
“retina,” the rear surface of the eye, which is lined with visual receptors. Light from the
left side of the world strikes the right half of the retina, and vice versa. Light from above
strikes the bottom half of the retina, and light from below strikes the top half. The
inversion of the image poses no problem for the nervous system. Remember, the visual
system does not duplicate the image. It codes it by various kinds of neuronal activity.

Route within the retina

In the vertebrate retina, however, messages go from receptors at the back of the eye to
“bipolar cells,” located closer to the centre of the eye. The bipolar cells send their
messages to “ganglion cells,” located still closer to the centre of the eye. The
ganglion cells’ axons join together and travel back to the brain. Many types of Amacrine
cells refine the input to ganglion cells, enabling certain ones to respond mainly to
particular shapes, directions of movement, changes in lighting, colour, and other visual
features.

One consequence of this anatomy is that light passes through the ganglion, Amacrine,
and bipolar cells en route to the receptors. However, these cells are transparent, and
light passes through them without distortion. A more important consequence is the
“blind spot.” The ganglion cell axons join to form the “optic nerve” that exists through
the back of the eye. The point at which it leaves (also where the blood vessels enter
and leave) is the “blind spot” because it has no receptors.

Fovea and periphery of the retina

When you look at details such as letters on this page, you fixate them on the central
portion of your retina, especially the “fovea” (meaning “pit”), a tiny area specialised for
acute, detailed vision. Because blood vessels and ganglion cells axons are almost
absent near the fovea, it has nearly unimpeded vision. The tight packing of receptors
also aids perception of detail.

The ganglion cells fin the fovea of humans and other primates are called “midget
ganglion cells” because each is smaller and responds to just a single cone. As a
result, each cone in the fovea has a direct route to the brain. Furthermore, many bird
species have two foveas per eye, one pointing ahead and one pointing to the side. The
extra foveas enable perception of detail in the periphery.

,Toward the periphery of the retina, more and more receptors converge onto bipolar and
ganglion cells. As a result, the brain cannot detect the exact location or shape of
peripheral light sources. However, the summation enables perception of fainter lights in
the periphery. In short, foveal vision has better “acuity” (sensitivity to detail), and
peripheral vision has better sensitivity to dim light.

2 List the properties of cones and rods

VISUAL RECEPTORS: RODS AND CONES

The vertebrate retina contains two types of receptors: rods and cones. The “rods,”
abundant in the periphery of the human retina, respond to faint light but are not useful in
daylight because bright light bleaches them. “Cones,” abundant in and near the fovea,
are less active in dim light, more useful in bright light, and essential for colour vision.
Because of the distribution of rods and cones, you have good colour vision in the fovea
but not in the periphery.

Both rods and cones contain “photopigments,” chemicals that release energy when
stuck by light. Photopigments consist of 11-cis-retinal (a derivative of vitamin A) bound
by proteins called “opsins,” which modify the photopigments’ sensitivity to different
wavelengths of light.

3 Explain the main features of colour vision

COLOUR VISION

We perceive the shortest visible wavelengths as violet. Progressively longer
wavelengths are perceived as blue, green, yellow, orange, and red. We call these
wavelengths “light” only because the receptors in our eyes are tuned to detecting them.
If we had different receptors, we would define light differently. Indeed, many species of
birds, fish, and insects have visual receptors sensitive to what we call ultraviolent
radiation. Of course, we cannot know what it looks like to them, but it certainly affects
their behaviour. In some species of birds, the male and females look alike to us, but
differently to birds, because the male reflects more ultraviolet light.

The Trichromatic (Young - Helmholtz) Theory

People distinguish red, green, yellow, blue, orange, pink, purple, greenish blue, and so
forth. Presuming that we don’t have a separate receptor for every possible colour, how
many types do we have?

The first person to advance our understanding on this question was an amazingly
productive man named Thomas Young (1773-1829). Young was the first to start
deciphering the Rosetta stone. Previous scientists thought they could explain colour by
understanding the physics of light. Young recognised that colour required a biological
explanation. He proposed that we perceive colour by comparing the responses across

,a few types of receptors, each of which was sensitive to a different range of
wavelengths.

This theory, later modified by Hermann von Helmholtz, is now known as the
“trichromatic theory” of colour vision, or the “Young-Helmholtz theory.” According
to this theory, we perceive colour through the relative rates of response by three kinds
of cones, each one maximally sensitive to a different set of wavelengths.
(“Trichromatic” means “three colours”). How did Helmholtz decide on the number
three? He found that people could match any colour by mixing appropriate amounts of
just three wavelengths. Therefore, he concluded that three kinds of receptors – we now
call them cones – are sufficient to account for human colour vision.

Given the desirability of seeing all colours in all locations, we might suppose that the
three kinds of cones would be equally abundant and evenly distributed. In fact, they are
not. Long – and medium – wavelength cones are far more abundant than short –
wavelength (blue) cones. Consequently, it is easier to see tiny red, yellow, or green
dots than blue dots.

The smaller the dot, the father you have to move it into your “visual field” – that is, the
part of the world that you see – before you can identify the colour.

The opponent - process theory

Stare at a colour under a bright light, without moving your eyes, for a minute. Then look
at a plain white surface, such as a wall or blank sheet of paper. Keep your eyes steady.
You will see a “negative colour afterimage,” a replacement of the red you had been
staring at with green, green with red, yellow and blue with each other, and black and
white with each other.

To explain this and related phenomena, Ewald Hering, a physiologist, proposed the
“opponent – process theory:” we perceive colour in terms of opposites. That is, the
brain has a mechanism that perceives colour on a continuum from red to green, another
from yellow to blue, and another from white to black. After you stare at one colour in
one location long enough, you fatigue that response and tend to swing to the opposite.

The retinex theory

The trichromatic theory and the opponent – process theory cannot easily explain
“colour constancy,” the ability to recognise colours despite changes in lighting. If you
wear green – tinted glasses or replace your white light bulb with a green one, you still
identify bananas as yellow, paper as white, and so forth. Your brain compares the
colour of one object with the colour of another, in effect subtracting a certain amount of
green from each.

To account for colour and brightness constancy, Edwin Land proposed the “retinex
theory” (a combination of the words “retina” and “cortex”): the cortex compares

,information from various parts of the retina to determine the brightness and colour for
each area.

Colour vision deficiency

One of the first discoveries in psychology was colour blindness, better described as
“colour vision deficiency.”

Colour deficiency results when people with certain genes fail to develop one type of
cone, or develop an abnormal type of cone. In red – green colour deficiency, the most
common form of colour deficiency, people have trouble distinguishing red from green
because their long – and medium – wavelength cones have the same photopigment
instead of different ones. The gene causing this deficiency is one the X chromosome.
About 8 percent of men are red – green colourblind compared with less than 1 percent
of women. Women with one normal gene and one colour – deficient gene – and that
includes all women with a red – green colour deficient farther – are slightly less
sensitive to red and green than the average for other people.

4 Trace the route of visual information from the retina to the cerebral cortex

Route within the retina

In the vertebrate retina, however, messages go from receptors at the back of the eye to
“bipolar cells,” located closer to the centre of the eye. The bipolar cells send their
messages to “ganglion cells,” located still closer to the centre of the eye. The
ganglion cells’ axons join together and travel back to the brain. Many types of Amacrine
cells refine the input to ganglion cells, enabling certain ones to respond mainly to
particular shapes, directions of movement, changes in lighting, colour, and other visual
features.

One consequence of this anatomy is that light passes through the ganglion, Amacrine,
and bipolar cells en route to the receptors. However, these cells are transparent, and
light passes through them without distortion. A more important consequence is the
“blind spot.” The ganglion cell axons join to form the “optic nerve” that exists through
the back of the eye. The point at which it leaves (also where the blood vessels enter
and leave) is the “blind spot” because it has no receptors.

5 Explain lateral inhibition in terms of the connections among neurons in the
retina

PROCESSING IN THE RETINA

At any instant, the rods and cones of your two retinas combined send a quarter of a
billion messages. You couldn’t possibly attend to all of that at once, and you don’t need
to. You need to extract the meaningful patterns.

,Actually, light striking the rods and cones “decreases” their spontaneous output.
However, they have “inhibitory” synapses onto the bipolar cells, and therefore, light on
the rods or cones decreases their inhibitory output. A decrease in inhibition means net
excitation, so to avoid double negatives, we’ll think of the output as excitation of the
bipolar cells. In the fovea, each cone attacks to just one bipolar cell.

Now imagine that light excites receptors 6 through 10. These receptors excite bipolar
cells 6 through 10 and the horizontal cell. Bipolar cells 6 through 10 all receive the
same amount of excitation. Bipolar cells 7, 8 and 9 are inhibited by input on both sides,
but bipolar cells 6 and 10 are inhibited from one side and not the other. That is, the
bipolar cells in the middle of the excited area are inhibited the most, and those on the
edges are inhibited the least. Therefore, bipolar cells 6 and 10, the ones on the edges
of the field of excitation, respond “more” than bipolar 7 through 9. Next, consider bipolar
cells 5 and 11. What excitation do they receive? None, however, the horizontal cell
inhibits them. Therefore, receiving inhibitation but no excitation, they respond less than
bipolar cells that are farther from the area of excitation.
These results illustrate “lateral inhibition,” the reduction of activity in one neuron by
activity in neighbouring neurons. Lateral inhibition heightens contrast. When light falls
on a surface, the bipolar just inside the border are most excited, and those outside the
border respond the least.

6 Define and give examples of receptive fields

FURTHER PROCESSING

Each cell in the visual system of the brain has a “receptive field,” an area in visual
space that excited or inhibits it. The receptive field of a rod or cone is simply the point in
space from which light strikes the cell. Other visual cells derive their receptive fields
from the connections they receive. This concept is important, so let’s spend some time
with it. Suppose you keep track of the events on one city black. We’ll call that your
receptive field. Someone else keeps track of events on the next block, another person
on the block after that. Now suppose that everyone responsible for a block on your
street reports to a supervisor. That supervisor’s receptive field is the whole street,
because it includes reports from each block on the street. The supervisors for several
streets report to the neighbourhood manager whose receptive field is the whole
neighbourhood. The neighbourhood manager reports to a distinct chief, and so on.

The same idea applies to vision and other sensations. A rod or cone has a tiny
receptive field in space to which it is sensitive. Some rods or cones connect to a bipolar
cell, with a receptive field that is the sum of those of the cells connected to it (including
both excitatory and inhibitory connections). Several bipolar cells report to a ganglion
cell, which therefore has a still larger receptive field. The receptive fields of several
ganglion cells converge to form a receptive field at the next level, and so on.

To find a cell’s receptive field, an investigator records from the cell while shining light in
various locations. If light from a particular spot excites the neuron, then that location is

, part of the neuron’s excitatory receptive field. If it inhibits activity, the location is in the
inhibitory receptive field.

Primate ganglion cells fall into three categories: parvocellular, magnocellular, and
koniocellular. The “parvocellular neurons,” with small cell bodies and small receptive
fields, are mostly in or near the fovea. (Parvocellular means “small celled,” from the
Latin root “parv,” meaning “small”). The “magnocellular neurons,” with larger cell
bodies and receptive fields, are distributed evenly throughout the retina. (Magnocellular
means “large celled”, from the Latin root “magn,” meaning “large.” The same root
appears in “magnify”). The “koniocellular neurons” have small cell bodies, similar to
the parvocellular neurons, but they occur throughout the retina. (Koniocellular means
“dust celled,” from the Greek root meaning “dust. They got this name because of their
granular appearance”).

The parvocellular neurons, with their small receptive fields, are well suited to detect
visual details. They also respond to colour, each neuron being excited by some
wavelengths and inhibited by others. The magnocellular neurons, with larger receptive
fields, respond strongly to movement and large overall patterns, but they do not respond
to colour or fine details. Koniocellular neurons have several functions, and their axons
terminate in several locations.
Axons from the ganglion cells from the optic nerve, which proceeds to the optic chiasm,
where half of the axons (in humans) cross to the opposite hemisphere. After the
information reaches the cerebral cortex, the receptive fields become more complicated.

7 Describe research on how experienced alter development of the visual cortex

THE PRIMARY VISUAL CORTEX

Information from the lateral geniculate nucleus of the thalamus goes to the “primary
visual cortex” in the occipital cortex, also known as “area V1” or the “striate cortex”
because of its striped appearance. If you close your eyes and imagine seeking
something, activity increases in area V1 In a pattern similar to what happens when you
actually see that object. If you see an illusion, the activity in area V1 Corresponds to
what you think you see, not what the object really is. People with damage to area V1
Report no conscious vision, no visual imagery, and no visual images in their dreams.

Some people with damage to area V1 show a surprising phenomenon called
“blindsight,” the ability to respond in limited ways to visual information without
perceiving it consciously. Within the damage part of their visual field, they have no
awareness of visual input, not even to distinguish between bright sunshine and utter
darkness. Nevertheless, they might be able to point accurately to something in the area
where they cannot see, or move their eyes toward it, while insisting that they are “just
guessing.” Some blindsight patients can reach for an object’s colour, direction of
movement, and approximate shape, also while insisting that they are just guessing.
Some can identify or copy the emotional expression of a face that they insist they do not
see.

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