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PSYC 304 > Vision > Flashcards

Vision Flashcards

1
Q

how is vision a selective, active process?

A
  • most visual information you get is void of colour (differences in wavelength)
    • most colour comes from the center of the eye, the fovea (macular)
  • eyes move around all the time, creating a higher resolution image
  • we construct mental world inside of our head
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2
Q

how and why does vision have a restricted range?

A
  • based on evolutionary usefulness: we see bands of light that are most useful to us
  • varies by species: insects see wavelengths that come off plants because it’s important to them
  • has a biological basis
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3
Q

what is adaptation?

A
  • constant information is ignored, or removed from consciousness because it is not important information
  • influences how the world is perceived in a personally useful way
  • we are not interested in absolute value, we are interested in relative value
  • explains why we don’t see the blood vessels in our own eyes
  • thus, we need constant eye movement (saccades) to prevent the world from fading
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4
Q

how does light travel into and through the eye?

A
  1. light comes in the eye
  2. moves through two lenses
    1. fixed - cornea
    2. flexible - lens (attached to muscles)
  3. ciliary muscles stretch or relax the lens to change the angle of light
  4. light travels through fluid
  5. passes through blood vessels and axons and cell bodies
  6. reaches photoreceptors that are in the inside back of the eye (retina)
  7. retina is next to the choroid - where the photoreceptors get their pigment
  8. photoreceptors require constant pigment in order to transduce a visual stimuli
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5
Q

what are the cornea and lens used for? how does this mechanism fail during dysfunction?

A
  • as the light strikes the cornea or lens, the angle of light changes to focus on the retina
    • cornea is fixed, but lens can stretch or relax based on muscles
    • lens allows us to focus on things closer or further away from us
  • in near-sightedness (myopia), the eye is elongated, retina is further back
    • lens causes light to converge before it lands on the retina
    • can be fixed by adding one more lens (glasses, contacts)
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6
Q

in what ways is our eye organized well?

A
  • many translucent layers (cells) to minimize how much light is scattering as it moves through
  • about 130 million photoreceptors per eye on the retina
    • most are cones but some are rods
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7
Q

how and where is the light signal transduced?

A
  • photoreceptors transduce light into neural activity
  • photoreceptors need pigment from choroid in order to transduce light in NS signal
    - if detached from the retina, cells run out of pigment and we are unable to see
  • light goes to rods and cones which transduce to → bipolar cells → retinal ganglion cells (RGCs)
  • horizontal cells are at synapses between photoreceptors and bipolar cells
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8
Q

how do cells responsible for vision differ in terms of action potentials?

A
  • photoreceptors: small cells, no action potentials; release neurotransmitters and have voltage changes
  • bipolar cells: short, no action potentials; release neurotransmitters and have voltage changes
  • horizontal cells: no action potentials
  • retinal ganglion cells: very long axons, action potentials; output from the eye to the thalamus; first place in retina to have action potentials
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9
Q

what types of receptors are used for vision? how do they work?

A

GCPRs
- GPCRs are sensitive to light and used in vision, much slower than if we had ionotropic channels
- rods and cones are at baseline, releasing neurotransmitters (glutamate) in the dark
- when light shines on the eye, it causes GCPRs to activate and inhibit neurotransmitter release, causing hyper polarization
- GCPRs are negative modulatory

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10
Q

how are rods and cones different?

A

Rods
- scotopic - low light conditions
- long, thin, cylindrical
- highly sensitive to light

Cones
- photopic - for seeing during the day
- short, thick, tapered
- less sensitive to light

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11
Q

how does the function of rods and cones determine where they are found?

A
  • in the fovea, we have lots of cones because they are used in daylight vision and colour
    • density decreases as you move away from the fovea which is why colour vision is really bad in the periphery
  • virtually no rods in the fovea, high density in the periphery
    • if you are out on a dark night, you should focus on area next to the star rather than right at it
    • because rods work in low light conditions and are better in the periphery
  • blindspot - where retinal ganglion axons move out of the eye
    • no rods and cones working here
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12
Q

how many rods do we have? how do they differentiate wavelengths of light?

A
  • about 120 million cells
  • all rods are sensitive to the same wavelength of light that is bluish/greenish
    • not good at differentiating between wavelengths of light (colours)
  • located everywhere except in the fovea
  • proteins in them are very sensitive to light, critical for vision at night (convergence - rods converge to a few bipolar cells)
    • explains why colour vision is poor in low light
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13
Q

how can rods become “bleached”?

A
  • easily “bleached” during the day: so active in the day that they use up all their pigment
    • vision is poor when you move from somewhere really bright to somewhere really dark
    • takes a couple minutes for rods to get their pigment back and start working again
  • important for perceiving movement and spacial information
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14
Q

how many cones do we have? how do they differentiate wavelengths of light?

A
  • about 7 million cells
  • less sensitive to light but are sensitive to wavelengths of light
    • three types of cones - sensitive to short, medium, and longer wavelengths of light
  • located mostly in the fovea
    • explains why the fovea is less useful at night
  • critical for perceiving colour
  • important for acuity, resolution, ability to see, mostly because they are abundant in the fovea
    • periphery is way more messy because all the axons and cells are pushed to the side so the fovea is clear
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15
Q

how do rods and cones work together to allow us to see colour?

A
  • there are sensitivity curves for different proteins on rods and cones
  • all rods have the same proteins, all are max sensitive to 400 nanometers wavelength (bluish-greenish light)
    • also sensitive to other wavelengths of light, but much less
  • different cones gives us a population (population coding)
    • pattern of activity across three types of cones gives us an idea of what wavelength of the light is
  • if we had more cones, we’d be better at distinguishing colours
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16
Q

how has vision differed from trichromatic vision across species and across time?

A
  • most mammals have dichromatic colour vision
  • dogs can see colours but their colour distinguishing is restrictive
    • can see shades of blue and yellow, but reds, greens, and yellows are indistinguishable
  • humans had four cone types in our history → became nocturnal → lost two cones (lost function of the gene)
    • eventually one non-functional colour gene became functional again (random mutations)
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17
Q

how does colour blindness occur in humans?

A
  • as a result of problems with the cone gene from the X chromosome which codes for long wavelength cone - red
  • men only have one X chromosome so if they have problems with long wavelength cone, they will have more trouble with seeing colour red
  • some individuals with two X chromosomes (XX) have two types of long wavelength cones, enhancing their ability to differentiate colors
  • protanopia - problem with seeing reds, long wavelength cone
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18
Q

what are some other kinds of colour-blindness?

A
  • deutranopia - problems with medium wavelength cones
  • tritanopia - problems with short wavelength cone
  • achromatopsia - complete loss of colour, see the world as black and white
    • usually a problem in the brain that affects colour perception, not a problem in the eye
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19
Q

can we input genes for cones to increase our perception of colour (acquired trichromacy)? what are the potential implications?

A
  • did gene therapy after animals’ development, added gene to the photoreceptors in the eye with surgery
    • they were able to see colours even though their brains didn’t have dedicated pathways for the new cone gene
  • brain can make sense of new information and new inputs
  • therapeutic implications - potential for helping colour blindness, even though it isn’t a huge deal for most people
  • science fiction implications - imagine adding new genes for cones to see new colours
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20
Q

what do parallel processing and convergence look like for vision?

A
  • parallel processing - same information being processed by different pathways
    • different information is picked up by different cells along different pathways (rods and three types of cones)
  • convergence - moving from many neurons to fewer neurons
    • rods converge to fewer bipolar cells, which converge to fewer retinal ganglion cells
    • retinal ganglion cells are output layer
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21
Q

what is the difference in amount of convergence for rods and cones?

A

lots of convergence for rods, almost no convergence for cones

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22
Q

what are the pros and cons of having high convergence?

A

this happens in rods
- pro: high sensitivity
- con: low acuity
- high convergence means that no matter where the light hits, the retinal ganglion cell will be activated (high sensitivity)
- but, retinal ganglion cell cannot determine where exactly the light came from (low acuity)

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23
Q

what are the pros and cons of having low convergence?

A

this happens in cones
- pro: high acuity
- con: low sensitivity
- when light strikes, we know exactly where it landed (high acuity)
- we are much less sensitive to stimuli (low sensitivity)
- less sensitivity is required anyways because cones are used in daytime

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24
Q

what are mach bands? what do they show us?

A
  • mach bands are a series of uniform bands next to each other that get lighter and lighter
  • we care about how the band looks in comparison to it’s neighbour, the edge that is next to a darker side will look lighter and the edge next to a lighter side will look darker
  • something that is flat gets a contrast enhancement, we are built to detect contrast, not to sense absolute values
  • organization and interpretation starts at the rods and cones (active process)
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25
Q

what are centre-surround organizations? what do they tell us?

A
  • lighter square with medium square in the middle or dark square with medium square in the middle
  • the medium square that is surrounded by the lighter square looks darker than the medium square surrounded by a dark square
  • centre-surround organization - centre influences the surround and the surround influences the centre
  • contrast enhancement happens first in the retina, helps us see where one thing ends and another begins
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26
Q

how is this centre-surround organization seen in the retina?

A
  • we record with action potentials from retinal ganglion cells to see contrast enhancement
  • the retinal ganglion cells have a centre-surround organization (donut shape)
27
Q

what are on centre, off surround cells?

A

cells that fire more if light arrives in the centre of visual field and less if it light arrives in the periphery

28
Q

what are off centre, on surround cells?

A

some retinal ganglion cells are inhibited if you shine light in the middle of visual field, and fire more when light arrives at the periphery

29
Q

why do we have receptive fields in vision?

A
  • neurons fire in some places and don’t fire in others
  • “on” center causes the cell to fire more, “off” surrounding causes the cell to fire less
  • helps us know exactly where a light is coming from
    • similar to how receptive fields of touch work
30
Q

how do ON and OFF channels work through lateral inhibition?

A
  • light is transduced into NS signal by rods and cones
  • they all converge into a bipolar cell (they don’t have action potentials)
  • they’re connected laterally as well, by the horizontal cell
  • they create an opponent process - when there is light shining in center, the horizontal cell prohibits firing in the periphery
    • and vice versa
  • this is lateral inhibition - cells that are in vertical pathways are connected laterally by horizontal cells
    • allows them to be mutually inhibiting, know where exactly the light is shining
31
Q

how does lateral inhibition occur in the retina?

A

using the mach bands example…
- despite being uniform in colour, the edges appear enhanced in contrast

  • each photoreceptor not only responds to light but also inhibits the activity of nearby photoreceptors

suppose there’s a border between a light grey bar and a dark grey bar
- the light grey side photoreceptors are more stimulated and inhibit their darker neighbouring photoreceptors more strongly -> makes the line appear darker
- the dark grey side photoreceptors experience less inhibition because their neighbors are receiving less light -> lrdd inhibition makes edge of the dark bar appear lighter
- creates a sharp contrast between the edges of the light and dark areas

32
Q

what is the optic nerve?

A

optic nerve is the axons from retinal ganglion cells

33
Q

does information from both sides of the world come into both eyes? how does this process in the brain?

A
  • each eye brings in information from both the left and right side of the world
  • the info that comes in from the right half of the world goes to the left half of the brain, and vice versa
    - but some axons stay on the same side that they came in
34
Q

what are hemi-retinas? where do they bring visual information in from?

A

hemi-retinas are described by how close it is to your nose vs. temples (medial vs. lateral)
- nasal-hemi-retina = closer to nose
- temporal-hemi-retina = closer to temples

35
Q

what is the optic chiasm?

A
  • where axons from the nasal-hemi-retina cross over
  • considered a tract and not a nerve bundle because it’s in the CNS
  • information from left visual field hits the nasal hemi retina on the left eye, must cross over to the other side
  • also info from the right visual field that hits the nasal hemi retina on the right eye
  • axons in the temporal hemi retina stay on the same side
  • signal goes from optic chiasm to lateral geniculate nucleus on the thalamus
36
Q

what would happen if we cut into the optic chiasm? what would this dysfunction be called?

A

cutting the optic chiasm = cutting where the nerves cross over
- bi-temporal hemianopia - can see the middle of vision but not the extreme outer edges of vision
- would lose the information coming from the nasal hemi-retina

37
Q

what is the lateral geniculate nucleus (LGN)? what are it’s layers like?

A
  • is a little bump on the thalamus that gets its input from the optic chiasm and projects to the primary visual cortex
  • has six layers that are consistently organized, some layers reflect info from left eye and some layers reflect info from right away
  • six layers are also parts of a different pathway, some layers get info from centre of vision (cones), while other layers get info from periphery of vision (rods)
  • organized according to whether it’s left eye or right eye, whether they are rods or cones, but also according to where things are following in the visual field
  • has a retinotopic map - adjacent parts of the visual field are represented by adjacent neurons
38
Q

what are the two different types of layers in the LGN and what are their pathways?

A
  • parvocellular layers of LGN - gets information from cones → bipolar cells → p cells → parvocellular layers of LGN
  • magnocellular layers of LGN - gets information from rods/cones → bipolar cells → m cells → magnocellular layers of LGN
  • p is for perception (shape, colour), m is for motion (grabbing attention because something is moving in the periphery)
39
Q

how does the LGN differ in number of layers for centre and periphery of vision?

A
  • centre gets 4 layers, periphery of vision gets 2 layers because the fovea is more important
  • even though there are more cells in the periphery layers
40
Q

what is the primary visual cortex?

A
  • receives its inputs from the lateral geniculate nucleus (LGN)
  • axons that project from the LGN to the primary visual cortex are part of the optic radiation pathway
  • also called V1, brodmann area 17, striate cortex (because it looks stripy)
41
Q

how does the primary visual cortex has a retinotopic map?

A
  • information in V1 is organized according to the retina
  • adjacent neurons represent adjacent parts of the visual field
    • these are not the same as reality
  • there is cortical magnification, most important things get the most amount of neurons in the brain
42
Q

what are simple cells in the primary visual cortex?

A
  • neurons that respond to specific features of visual stimuli, such as orientation, position, and spatial frequency
  • are especially sensitive to orientation and movement of lines in the visual field
  • simple cells have center-surround receptive fields, some have an on centre, off surround, while others have an off centre, on surround
  • fire most strongly when a line in their receptive field is oriented in their preferred direction (vertical, horizontal, diagonal)
43
Q

how were simple cells first discovered in the primary visual cortex?

A
  • researchers had difficulty getting cortical neurons to fire above baseline when presented with regular dots
    - made it challenging to identify their receptive fields
  • movement of a line across the visual field caused these cells to fire
  • shows that the cells in the cortex are sensitive to more complex visual fields (lines)
44
Q

what are ocular dominance columns?

A
  • groups of neurons are organized in columns, and each column is responsive to input from either the left eye or the right eye
  • columns are usually alternating, which helps with binocular vision and depth perception
  • looks like a striping pattern, part of the reason why we call the primary visual cortex the striate cortex
45
Q

how did we first discover ocular dominance columns?

A
  • portal or window was made at the back of the head then infrared light was shone onto the brain to observe BOLD activity
  • when light was shone into one of two eyes, a distinct striping pattern was observed in V1
  • pattern indicated that different parts of the cortex were receiving input from either the left or right eye, and both eyes are processed separately
46
Q

in what ways are ocular dominance columns flexible?

A
  • if you wore an eye patch, the eye that was covered would show a reduction in the size of its associated column, while the uncovered eye’s column would become more dominant
  • the structure of ocular dominance columns can change depending on visual input
  • flexibility is more prominent during early life
47
Q

what are orientation columns?

A
  • vertical columns of neurons in V1 that are sensitive to specific orientations of lines or edges in the visual field
  • means different neurons within a column respond to different angles of lines, such as horizontal, vertical, and diagonal orientations
  • simple cells form the basis of orientation columns because they share a similar response to specific line orientations
  • visual cortex is organized not only by orientation but also by colour sensitivity, ensuring that both aspects of visual stimuli are processed in parallel
48
Q

is colour perception just wavelengths?

A
  • things can be the same wavelength of light but we will still perceive them as different colours
  • colour is a mental phenomenon that requires a lot of processing and interpreting
    • banana looks yellow under all lighting conditions
49
Q

what are the two theories/stages of colour?

A
  1. Young-Helmholtz Trichromatic Theory
  2. Hering’s Opponent Processing Theory
50
Q

what is the Young-Helmholtz Trichromatic Theory?

A
  • all colours can be produced through a combination of red, green, and blue
  • if you shine all three together, you see white light
  • suggests that our eyes have three types of colour receptors (3 cone types)
51
Q

what is the Hering’s Opponent Processing Theory?

A
  • theory suggests that colour perception is based on opposing pairs of colours, meaning the brain processes certain colours in opposition to one another
  • red → ← green, yellow →← blue, white →← black
  • instead of seeing colours independently, the brain compares them to each other in a competing process
  • signal converges in specialized cells in the brain that compare the info from different wavelengths of light
    • ex. when light of medium wavelength (green) and long wavelength (red) are detected by cones, medium wavelength = inhibitory and long wavelength = excitatory, creates the perception of a balanced colour
  • we have long cone centre, medium cone surround
52
Q

do these two theories sufficiently explain the perception of colour?

A
  • these two theories alone are still insufficient, a lot of colour perception is top-down
  • we know oranges are orange, we know bananas are yellow, we use this information for perception
  • perceptual constancy - easier to make sense of the world since our perception is constant
53
Q

after the primary visual cortex, where does visual information go?

A

can take two different streams
1. dorsal stream - to posterior parietal cortx
2. ventral stream - to inferotemporal cortex

54
Q

where is there convergence and where is their divergence when it comes to vision?

A

convergence at the cones, divergence in the brain (dorsal or ventral stream)
- we need parallel processing to be able to perceive something
- need to know colour, motion, distance, etc. which are all processed in different brain areas

55
Q

what do the different pathways from the primary visual cortex do?

A
  • dorsal pathway (how) - discriminating according to where things are in space; movement, depth space
  • ventral pathway (what) - discriminating what things are; interested in colour, shape and form, sophisticated things like faces
56
Q

what study showed how damage to the dorsal vs. ventral pathways affect vision differently?

A
  • two tasks (1) object recognition, pick the new object (2) spacial recognition, pick option that is closer to an object
  • monkeys that have damage to posterior parietal cortex (dorsal pathway) have problems with spacial recognition
    • can’t differentiate which object is closer to another
    • can still recognize which object is new
  • those that have damage to inferotemporal cortex (ventral pathway) have problems with picking the object that is new
    • can’t differentiate between new and old objects
    • can still perform well on spacial recognition
57
Q

what was the study that tested whether people with vision problems could judge the orientation of a line?

A
  • patient DF (damage to ventral stream) - could not visually identify the orientation of a line
    • what is the angle of the mailbox slot? couldn’t visually identify
    • if you give them something like mail and ask them to slot it, they can do it
    • this is why the dorsal pathway gets referred to as the “how” pathway
58
Q

is the halle berry neuron a visual neuron?

A
  • halle berry neuron is in the inferotemporal cortex (part of ventral pathway)
  • is involved in visual perception, as it responds to visual stimuli such as faces or pictures
  • not only a visual neuron, it represents a higher-order cognitive process where visual information is integrated with memory and conceptual knowledge to help us recognize objects and faces
  • shows how high levels of perception and recognition of faces requires memory
59
Q

is it possible to have non-conscious vision?

A
  • it wouldn’t be vision because we aren’t consciously seeing anything or using vision for explicit cognitive processes
  • but it is possible for some information from light and vision to be processed even if the person doesn’t have conscious vision
60
Q

how do people with a loss of vision still experience circadian rhythms?

A
  • loss of vision doesn’t lead to loss of circadian rhythm even though light is the main thing that synchronizes our circadian rhythm
  • in our eyes, we have special retinal ganglia cells that have photoreceptors on them
    • travel in a different pathway, not part of the visual pathway
    • pick up light signals and axons project to hypothalamus (superchiasmatic nucleus) instead of thalamus
  • allows light to synchronizes circadian rhythms of people with congenital problems with rods and cones
61
Q

how do people with occipital lobe (V1) damage still use visual information?

A
  • people who have severe V1 damage and can’t consciously see, but their eyes are still intact, can use visual information
    • they can guess stimuli presented to them with higher-than-chance accuracy
    • not consciously aware of what they’re seeing, but it’s still impacting their choices
62
Q

what is “blindsight”?

A
  • where individuals with damage to the primary visual cortex (V1) can still perform certain visual tasks without consciously seeing anything
  • they have been seen to be able to navigate a room with obstacles
    • driven by the superior colliculi - gets visual information and uses it to orient head and eye movement
    • even though we aren’t consciously aware, it still guides behaviour
63
Q

in what way is the visual system a great model for the central nervous system?

A
  • vision is an active process, not passive
  • vision is relative, not absolute
  • lots of parallel processing
  • convergence and divergence
  • contralateral, topic organizations

PSYC 304 (10 decks)

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