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PHGY 314 > Visual (Pack) > Flashcards

Visual (Pack) Flashcards

1
Q

What are the 2 main functions of the eyeball?

A

Eyeball acts as a camera:
- Focus light → cornea + lens
- Capture images

*1 point in the world = 1 point on the retina
*2 points in the world = 2 points on the retina separated by an “equivalent” distance as in the world

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2
Q

How is the cornea limited?

A

The cornea has a static shape → limited focal range

The lens acts in very close and far focus → lens is attached to ciliary mucles
*Lens have voluntary and inoluntary control

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3
Q

What are the most common optical defects?

A

Astigmatism → the lens or cornea are not spherical
- Myopia = eyeball is too long
- Hyperopia = eyeball is too short
*Causes 1 point in the world to appear as 2+ points on the retina

Prebyopia → the lens gets stiff and is unable to accomodate for near vision

Cataract → changes in lens color (milky white deposits in the lens)
- Congenital or with aging
- Resolved by surgery

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4
Q

Which cells are found in the retina? (In what order?)

A

Light → Retinal Ganglion Cells → Amacrine cells + Bipolar cells → (Horizontal cells) → Photoreceptors

*The retina is inverted

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5
Q

What are the 2 kinds of photoreceptors and their characteristics?

A

*Only part of the nervous system to deal with light
Rod → Scotopic vision
- 20x more than cones
- long thin
- Highly sensitive to light (activated by 1 photon)
- Specialized for night vision → saturate in daylight
- Low temporal resolution
- Low spatial resolution
- Color-blind
- Common in peripheral vision (none in fovea)

Cones → Photopic vision
- short large
- Less light-sensitive (activation threshold ~100 photons)→ specialized for day vision (saturate only for very intense light)
- High temporal resolution
- High spatial resolution
- Chromatic
- Common in foveal vision

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6
Q

What wavelengths correspond to the visual spectrum?
How does this relate to photoreceptors?

A

Visible Spectrum = 400nm - 700nm

400nm = Purple → blue
700nm = Red

*Each photoreceptor is sensitive to a limited range of wavelengths (corresponds to particular colors)
Most people have 3 cones: Blue (most sensitive to 420nm), Green (531nm), Red (558nm)
Color-blind people have 2 cones: Blue, Red-Green
*They are less activated by wavelength that are further from peak wv

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7
Q

What wavelength best activates rods?

A

500nm
*NOT color sensitive, just better activated by this wavelength

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8
Q

How does each photoreceptor individually respond to different light intensities?

A

Each photoreceptor has a range (curve)
Below threshold, changes in light intensity don’t really change the output
Over saturation level, changes in light intensity don’t really change the ouput of the photoreceptor

Between Threshold - Saturation (small window) → increase in light intensity leads to increase in photoreceptor response (more hyperpolarization in membrane potential)
→ Ralative to a dark envrionment baseline current, photoreceptors change their membrane potential about - 40mV (increased response = decreased membrane potential)

*Each photoreceptor has a different threshold/saturation point that complements others

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9
Q

What are the 3 levels of vision from most light → darker?

A

Retinal damage because too much light → Photopic vision → Mesopic vision → Scotopic vision (legally blind) → Dark

*Rod saturation = when its almost too dark to read letters on white paper

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10
Q

Why is light adaptation required?
What happens at the molecular level that allows for light adaptation?

A

It would take too many photoreceptors to cover the whole range of light intensities with such small response windows → the same photoreceptor need to be modulated to increase and lower the thresholds depending on environment

*Occurs over a peiod of seconds, involves chemical changes within the photoreceptors → increase in the levels of cGMP → allows opening of more Na+ channels even in more bright conditions (as if it was darker) → restores membrane potential (to a more depolarized)

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11
Q

How does the photoreceptor get activated in light vs dark at the molecular level?

A

Photoreceptors have Na/K pump
Dark:
transducin is bound to G protein (chills) → high cGMP levels → keeps Na+ channels open (coming in) → keeps the membrane potential depolarized (-40mV)

Light:
Transducin G protein cascade activated → decreased levels of cGMP → Na+ channels are closed → no more Na+ coming in, but K+ going out → hyperpolarization of the membrane potential (-70mV)

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12
Q

What are the 2 main consequences of light adaptation?

A

1) Cells are largely unresponsive to uniform light → they respond to the difference between light at a point and mean luminance in the neighbourhood around that point

2) Brightness measurements are RELATIVE (not absolute)

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13
Q

What is the main role of retinal ganglion cells?
What is their input/output like?

A

They allow communication of the visual information to the brain → ouput of the retina

They receive their input from bipolar cells, commnicate by firing Action Potentials (unlike photoreceptors which communicate in graded responses)

Axons of the ganglion cells form the Optic Nerve

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14
Q

What is the difference between the firing response of the receptive fields of achromatic vs colour-opponent retinal ganglion cells?

A

Both ON-center/OFF-surround or OFF-center/ON-surround

Achromatic RGC = amount of ON-center + amount of OFF-surround

Chromatic RGC = amount of RED-center - amount of GREEN-surround
*If not Green surround → still firing for red center

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15
Q

Explain the Hermann Grid Illusion (1870).

A

Grid with black squares + white row/columns in between → Intersections appear darker than rest of the white

Explanation: ON-centered ganglion cell responses are weaker at the intersections because they are negatively stimulated from the off-surround (more light in the surround → inhibition in the intersections than in the straights)

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16
Q

How would an ON-Center/OFF-surround RGC fire in response to a big white patch?

A

No change in the baseline firing → activation due to the light in the center is cancelled out by inhibition due to light in the surround

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17
Q

How would an OFF-Center/ON-surround RGC fire in response to a light array specifically in the center?

A

Baseline firing would be shut off (inhibited) / cell is silenced
*Pattern is the opposit as what the cell wants

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18
Q

How would an RED-Center/GREEN-surround RGC fire in response to a big red patch in its RF?

A

It would have an increased firing rate as it is sensitive to the red in the middle (and not inhibited by the red outside)
(Red surround - Green surround)

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19
Q

How would an RED-Center/GREEN-surround RGC fire in response to a smalle green array in the center? To a large green patch?

A

Green in the center of the → basal firing rate

Green in the whole RF → Cell is silenced (inhibition)

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20
Q

What is the cause of most color blindness (deuteranomaly)?

A

A mutation shifts the medium wavelength cone towards the red end of the spectrum

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21
Q

What is the colour-opponent theory?

A

Perception of colour is linked to neurons (ganglion) that measure the DIFFERENCE between activity in different cone type, not comparison of individual photoreceptor input (green vs red / yellow vs blue)
→ Double-opponent blob cells in V1
Also related to assumptions about the environment

*Yellow = G + R
→ Green has lower wavelength so negative in relative visual sensitivity (red = positive)
→ Blue has lower wavelength so negative in relative visual sensitivity (yellow = positive)

*Retinal ganglion cells have opponent responses to different wavelengths

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22
Q

What illusion can colour-opponent theory cause?

A

Adaptation (photoreceptor fatigue) can reduce the inhibitory influence of one cone type → perception of the opposing colour, even when no colour is actually present

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23
Q

What are 2 kinds of ganglion cells?
(not chromatin and achromatic)

A

Mangnocellular:
- low spatial resolution
- High temporal resolution
- Color blind
- Located outside the fovea
- Large receptive field → stimulated by rapid changes over time (motion)

Parvocellular:
- High spatial resolution (details)
- Low temporal resolution
- Color-sensitive
- Common in fovea
- Small receptive field → concerned with fine spatial details (form) → assemble to make precise images

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24
Q

What part the visual fields is in whic side of the brain visual cortex?

A

Left side of visual field → Right brain visual cortex
Right side of visual field → Left brain visual cortex

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25
Q

Where does information on the far left vs on the middle/right side of the visual field gets processed by the left eye? What path does it follow?

A

Far left side → right side of the retina → crosses at the optic chiasm → Right lateral geniculate body → right visual cortex

Middle/right → left side of the retina (bc on the “right” side of the left eye) → stays on the left at the optic chiasm → left LGN → left visual cortex

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26
Q

What lesions would cause the following defects in visual fields:
- Whole right eye
- Outside half of each eye’s visual field
- The left half of each eye
- the top left corner of each eye

A

Whole right eye → lesion in the optic nerve
Outside half of each eye’s VF → Optic chiasm
Left side of each eye’s VF → Right optic tract
Top left corner of each eye → in the cortex passed the LGN

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27
Q

What type of RGC are all the chromatic cells?

A

They are all parvocellular
(but all parvocellular are not chromatic)

28
Q

How are lateral geniculate neurons’ receptive fields similar to retinal ganglion cells?

A

2 main morphological types → parvocellular and magnocellular
Parvocellular → color or black/white
Magnocellular → colour-blind
2 different responses to light/cell → on-center and off-center

29
Q

What is the structure of the LGN like?

A

Made of 6 layers (6 on the outside, 1 inside):
6 - 3 = parvocellular neurons
2 - 1 = magnocellular neurons

Eye correspondance: (If talking about left LGN)
6 - Contralateral (right eye)
5 - Ispilateral (left eye)
4 - Contralateral
3 - Ipsilateral
2 - Ispilateral
1 - Contralateral

30
Q

What happened when the magnocellular neurons of the LGN were inactivated via chemicals (to simulate lesion)?

A

Magnocellular lesions impair the perception of fast-moving stimuli
Before lesion, contrast sensitivity did not decrease with increasing velocity
After lesion, contrast sensitivity significantly decreased with increasing velocity
*Velocity = deg/sec

31
Q

What is sinewave grating?

A

It allows to give a sensitivity score

Stimulus = A*sin(wx)
- A controls the contrast of the stimulus → contrast sensitivity describes how observe can see or not dimer gratings

  • w controls the spatial frequency (width of the bands) → spatial sensitivity describes how observe can see gratings of different width

*Contrast sensitivity is different for different spatial frequencies (at optimal with, we can see dimer bands for example)
*Similar effects seen for temporal frequencies of different contrasts

32
Q

What equation allow for measurement of the velocity of a grating?

A

Velocity = Temporal frequency/spatial frequency
→ Increasing temporal frequency increases velocity
→ Increasing spatial frequency decreases velocity

33
Q

What is the effect of a lesion in the parvocellular LGN?

A

*Test on static grating → Contrast sensitivity x Spatial frequency

Magno lesion had no effect because static
Parvocellular lesions reduced sensitibity to gratings, and completely eliminated color perception
*At higher temporal frequencies, when you start moving, parvo lesion shows better contrast frequency that magno lesion
*Magno is not responsible for color so no color discirmation when lesions

34
Q

What is the Superior Colliculus?

A

The retina projects onto the SC ~10% of the output of the retina
- Most receptor fields have center-surround organization (as in retina and LGN)
- Direct input comes primarily from magnocellular retinal ganglion cells → SC

*Faster processing, not affected by lesions that can occur in stroke patients for example
→ Unconscious processing as stroke patients say they don’t see, but will often be able to guess the number of fingers

35
Q

What are the properties of blindsight?

A
  • Does not reach awarness (mostly)
  • Activated by large stimuli
  • Most effective for low spatial frequencies and high temporal frequencies (moving, not many details)
  • Little sensitivity to color
36
Q

What are the main characteristics of the retinotopic map in V1?

A

Projections from LGN → V1 is retinotopic:

  1. Neurons that are physically near each other respnd to similar parts of the visual space
  2. Center of the visual field (at the fovea) → largest area in V1
  3. Periphery of visual field (largest area on the retina) →smallest area in V1
  4. Absolute opposit arrangement: top-left in the visual field (middle) → bottom-right in V1
    *Independent of the eye of origin
37
Q

What is the cortical magnification factor?

A

The size of an object ~ size of the angle it covers on the retina (degrees) → cortical magnification factor = amount of mm in cortex occupied by object of a given size (degrees)
Mc = A/(E + k) → farther object = smaller
E = position on retina (= 0 in the fovea), bigger E (further) → smaller Mc
A and k = constants

*The number of neurons in the visual cortex responsible for processing the visual stimulus of a given size varies as a function of the location of the stimulus in the visual field
*The visual cortex over-represent the input from the fovea

38
Q

What equation relates the size and space of the object and its place on the retina?

A

Tan(Θ/2) = (x/2)/d

39
Q

Which layer of the visual cortex receives all the input from LGN?
How is it organized?

A

Layer 4C
Alternance of information from right and left eye → occular dominance columns
Layer 4C alpha → projections from magno cells
Layer 4C beta → projections from parva cells

*Same in right and left cortex independently

40
Q

Where does information from layer 4C project in V1?

A

4C → upper layers → extrastriate cortex (higher areas of visual processing)

4C → layer 5 → superior colliculus in the sub cortex
4C → layer 6 → Feedback to LGN (not really understood because only input to V1 comes from LGN)

41
Q

Where do layer II/III, V, VI project to in the cortex and in V1?

A

II/III → cortex → V2, V3 (extrastriate visual areas)
V → subcortical → superior colliculus
VI → thalamus (feedback) → LGN

*Extrastriate visual areas = V2, V3, V4, V5, etc. have different specific functions in information processing

42
Q

What are the characteristics of simple cells in V1?

A

1 cell has separate receptive-field regions that respond to light and dark stimuli (ON/OFF regions)→ orientation tuning of a simple cell can be predicted from its response to small spots of light

Receive input from multiple LGN → have edge sensititivity
*1st type of orientation-selective cells

43
Q

What are the characteristics of complex cells in V1

A

*2nd type of orientation selective cells
- NO separate subregions (no OFF regions), only orientation selectivity
- Respond equally to light and dark stimuli all over the RF
- Can’t predict response to complicated stimuli by studying the spatial structure of RF (testing with light stimulus)
→ Information about orientation, not local contrast
Simple cells (RFs) with same orientation, but opposit ON/OFF arrangement sum up → input on Complex cells to make their RFs

44
Q

What was oberved when Hubel and Wiesel put an electrode in V1 at different depth and orientations?
(Put the electrode straight down vs in an angle)

A

When put the electron straight down → neurons respond to same orientation (orientation colum)

When in an angle → gradual/smooth change in prefered orientation (not random)

Conclusion: 3D arrangement with 1 axis being Orientation columns, other Occular dominance columns, other being different layer of V1

45
Q

What was observed when later doing optical imaging of of V1 (what is the name of the model observed in contrast to square map from Hubel and Wiesel)?

A

Pinwheel model of the visual cortex:
Instead of being a square, ‘circular’ region corresponding to different region in visual field had a continuum for different orientation sensitivities with convergence in the middle

*With single cell resolution, they where able to see that the brain has a spatial map a the single neuron level
*Different orientations activate different neurons but at equal levels

46
Q

How is the orientation map developped?
What happens at the level of the brain when someone looses their eye as an adult?

A

It is developped based on experience in the first 3 years of life → requires normal early development and stimulation

When someone looses their eye as an adult → not enough plasticity to remodel that area → occular dominance columns stay there chilling

47
Q

What are Blobs?
What are the characteristics of Blob cells?

A

Blobs are additional column systems → selective for color, not orientation
- Found in columns in the upper layers of V1 (mostly in layers 2/3)

Blob cells are double-opponent → Red+Green- center / Red-Green+ surround
*Opponent collor is inhibitory of that part of the RF, similar to achromatic cells

48
Q

What is simultaneous color contrast?

A

Refers to the tendency of the visual system to perceive colors in a way that depends on the color that surround them

49
Q

What is the definition of an orientation column?

A

Run perpendicular to the surface of the cortex
Each cell in the column is tuned to the same orientation

50
Q

What is the definition of an occular dominance column?

A

Run perpendicular to the surface of the cortex
In layer 4C cells, respond to input from only 1 eye (as in the LGN)
In the other layers, cells are binocular but still respond more to one eye than to the other

51
Q

What is the definition of hypercolumns?

A

Hypercolumns contain orientation columns representing 180˚ of orientations and occular dominance columns corresponding to both eyes

Within a single hyper column, neurons have receptive fields that represent similar locations in space

Hypercolumn structure in repeated across the visual cortex for every part of visual space
*Was seen to actually be more pinwheel instead of square columns

52
Q

Which of the LGN cells or Blob cells are more important for color contrast perception?

A

Blob cells because they are double-opponents (LGN cells are single-opponents)
- LGN have excitatory response to one colour in the center and inhibitory reponse to opponent colour in the surround
- Blob cells have excitatory response to one colour in the center + opposing colour in the surround. The opponent colour is inhibitory in each part of the RF

53
Q

For the illusion of the blue-black vs yellow-white dress, what explains the differences in perceptions?

A

Hypothesis: People perceive a combination of physical light characteristics (wavelengths) and their own assuption about the backgroud illumination

If see bright background → see blue-black
If see dark background → see yellow-white
*in contrast

54
Q

What are different type of selectivities cell can have in the visual cortex?

A
  • Orientation
  • Motion direction
  • 3D depth (binocular disparity)
  • Stimulus length
  • Colour-opponency
55
Q

What type of input do the motion direction selective cells in the visual cortex get?

A

Follows the simple cell model:
Motion direction selective cells would receive input from 2 rows of LGN → 1st row would respond faster, 2nd row would have a delay in the response (both rows selective for the same orientation)
I the line goes through delayed row 1st and then quick row → input gets to the V1 cell at the same time → LGN input arrives synchronously to the simpel cells → more firing

If the line goes in the other direction, the quick bursting will cause small 1st wave of firing from V1 cells and delayed will cause 2nd later wave of firing

→ Motion Direction selectivity is constructured from LGN inputs that are shifted in space and delayed in time

*By adding a spiking threshold, you can account only for when the activity is synchronous
*motion direction selective cells of the visual cortex are also orientation selective

56
Q

What is the Aperture problem?

A

Local measurements of edge motion are one-dimensional → you can’t know if the diagonal line is moving upwards or left/rightwards

V1 neurons see the component of motion perpendicular to the orientation of an edge → they prefer perpendicular movement

For moving object, the measurements of velocity in V1 will differ depending on the orientation of the object’s edges (higher velocity of moving perpendicular to the orientation of the line)
*Prefered

Aperture problem causes the V1 cells to often signal the wrong direction of motion → ability of V1 to communicate information about velocity is limited

57
Q

How does our brain know about depth?

A

The brain uses different cues to estimate depth:
- Smaller ~ Farther
- General knowledge
- Converging lines ~ father in depth

58
Q

What is binocular disparity? What does it allow?

A

Binocular disparity is the difference between the 2 different points stimulated in the 2 retinas.

Focus center → Fovea of each eye
The spot on which an object appears on the retina of each eye compare to the fovea tells if farther or closer

Far disparity → on the inside of the fovea of each eye (smaller angle to cornea)
Near disparity → on the outside of the fovea (bigger angle to cornea)
*Relative to the plane of fixation

59
Q

What cells in the visual cortex allow for binocular disparity information processing?

A

Some cells in V1 have specific selectivities:
- Tuned near
- Tuned zero
- Tuned far

60
Q

What input do V1 cell selective for binocular disparity receive? (How is the input from LGN organized)

A

V1 cells receive input from a column of left-selective LGN (from one eye) and a layer of right selective LGN (from the other eye) → The sum of these will lead intense firing

Selectivity for binocular disparity can be found in simple cells whose LGN inputs have slightly different receptive field positions in the 2 eyes (1/2 are left selective from 1 eye and 1/2 is right selective from the other eye)

61
Q

What is the binocular disparity of the plane of fixation?

A

ZERO → the object appears in the fovea of both retinas
*By definition

62
Q

What is endstopping?
When is it useful?

A

Horizontal inhibitory connections → useful for curvature detection
- Reduced response to long edges compare to short edges
- Highest response if the edge stops at the edge of the neurons RF (not the shortest the most)

*Selectivity of V1 cells for stimulus size

Very useful to detect curvature !! (due to inhibition of long edges) → curvature gives lots of information on shapes

63
Q

What model explains endstopping in V1 cells?

A

Size tuning involves inhibition from neighbouring neurons, but too complex to understand with a simple input → output explanation
*Horizontal connected across several hypercolumns

64
Q

What is contour integration?

A

It is another type of selectivity of some V1 cells
→ Allows lines of similar orientation to stand out against a background of random orientations

It involves excitation among neighbouring neurons (opposit of size tuning)

65
Q

What are horizontal connections? What is their importance?

A

Horizontal connections are anatomical projections from 1 cell to another within V1
- Span distance of several millimeters → link hypercolumns corresponding to different parts of visual space
- Link cells with similar preferences or orientation/colour (blob cells connect to blob cells and orientation selective to similar orientation-preferences)
- Horizontal connections can be inhibitory (enstopping) or excitatory (contour integration) → curvature detection

PHGY 314 (8 decks)

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