VISION Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

WHAT IS THE THEORY OF EXTRAMISSION?

A

the idea that they eyes can go out of the body and reach to obtain vision

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2
Q

democtrius on vision?

A

changes produced in the soul (brain), eyes alone, atoms, visual images are blurred but prossesed by the brain

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3
Q

Alhazen

A

moved vision understanding forward - things dont come out of the eye - lights rays go ito the eye - white light has many colours and visual illusions

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4
Q

da vinci

A
  • images are projected upside down on the retina
  • drawings
  • disections
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5
Q

hermann von helmholtz

A

opthalmoscope - candle and mirrors reflect the light so we can see at the back of the eye
vision is a learning process

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6
Q

cornea

A

main lens

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7
Q

Aqueous humour

A

fluid in anterioir chamber

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8
Q

iris

A

eye muscle - colour

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9
Q

pupil

A

hole in iris

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10
Q

Vitreous humour

A

jelly between lens and retina

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11
Q

what is shed at the back of the eye

A

disk cells are shed at the back of the eye in order to prevent us from becoming blind they are taken in the blood stream

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12
Q

fovea

A

central part of the visual field

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13
Q

foveal pit

A

clear and sees light

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14
Q

cone cells

A

colour vision and high resolution vision, 6 million cones, gives you sharp colour vision in the light

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15
Q

rod cells

A

non in the centre of vision, no blue cnesin the centre, more red than green. 100 million rods, sensitive to light, low res blurry black and white night vision

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16
Q

what is the optic disk

A

transfer signals from the photoreceptors of the eye to the optic nerve, allowing us to see

round spot on the retina formed by the passage of the axons of the retinal ganglion cells

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17
Q

what does visual angle refer to

A

size of something on the retina

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18
Q

where is our visual blind spot

A

around 15 degrees from the centre

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19
Q

what is lateral inhabition

A

this is when excitatory inputs inhiit neighboring neurons, this neables constrats in lighting to be more noticeable.

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20
Q

myopia

A

shortsightedness
images dont project close enough to the reitina

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21
Q

hyperopia and presbyopia

A

long sightedness

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22
Q

glaucoma

A

Damage to the nerve cells (wiring) because of high intraocular pressure

aqueous humour cannot drain from eye
angle between iris and cornea is closed

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23
Q

macular degeneration

A

Degeneration of the retina and death of the photoreceptors (sometimes accompanied by leaking blood vessels) – often age-related

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24
Q

some who cant see in their perihperal vision is lilely to have …

A

glaucoma

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25
Q

diabetic retinopathy

A

blood vessels start leaking blood into the eye in patches. treat by burn blood vessles with a laser, stop blood vessels from leaking,

black dots in vision but youd typically fill these in with ur brain

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26
Q

newtons prism experiment

A

newton put white light through a prism and it refracted a rainbow he then put this light into another prsim and this did not divide into more colours suggesting taht this colours are all that there is

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27
Q

what did netwon find

A
  • white light is a mixture of wavelengths (different colours)
  • Refraction (bending) depends on wavelength,
  • Object color depends on the lighting
  • You can mix ‘primaries’ to produce any other color
  • In other words, he described the physics of color
28
Q

what did thomas young conclude?

A
  • he postulated the theory of trichromatic vision
  • three retinal phtoreceptors produce all our color vision
  • limited colour receptors on the retina
  • 7 distcintcions from these
29
Q

what was thomas youngs research on the retina and what did he find?

A
  • the eye is a wobbly jelly which is hard to look at
  • use laser to produce opposite wobbly effect so eye is straight
  • can then look at cones
  • eventhough we all percieve colour in the same way our cones vary
30
Q

what do the cones detect

A
  • they detect wavelengths in terms of LMS long medium and short
  • not in terms of red green and blue
31
Q

what is metamerism?

A
  • many spectra will give rise to the same colour
  • the percieved matching of colours with different spectra
32
Q

what is opsin gene?

A

code for pigements that absorb light and as these pigaments aborb light they changed the way photoreceptors activate themselves - signal down to the brain - these determine wether LMS light is abosrbed

33
Q

describe human chromsomes

A
  • Humans have 23 chromosome pairs (think “23 and me!”).
  • In almost all cells they come in pairs (‘diploid’).
  • Germ-line cells (sperm, eggs) are ‘haploid’: one of each type.
  • The sex chromoxomses (‘X’ and ‘Y’) are special
34
Q

where does colour receptor gene sit

A

on the x chromosome

35
Q

which cone is the rarest

A

s cone - blue cone - is so rare that it is unlikely that you would have blue-yellow colour blindness

36
Q

what genes/cones is colourblindness most often caused by

A

l and m opsin genes

37
Q

why do l and m most often cause colourblindness

A

L AND M genes are very close not evenly spaced on absortion spectra so these convey almost same info

38
Q

so what is colourblindness

A
  • M cones become L
  • the L - M dimensions disapears
  • still discriminate between dark/light and yellow/blue
  • but not between red/green
39
Q

animals cant discriminate between ..

A

red and green
anomalous trichromacy - were red and green dimenesion is poor

40
Q

what is dichromacy

A

l or m are absent

41
Q

what is the rarest colourblindness

A

tritanopia - lack s cones (blue)

42
Q

what were our primate ancestors

A

dichromats l or m absent

43
Q

what is the ventral stream?

A

seems to be concerned with object identity and ‘form’. It has a strong representation of the fovea and a strong response to color

44
Q

what is the dorsal stream?

A

The ‘dorsal stream’ seems to be involved in motion, action and location. Some regions here (like hMT) respond very weakly to pure color

45
Q

neurons and colour

A

Some cortical neurons (and areas) have strong biases for colour or luminance stimuli

46
Q

Describe neurons range

A
  • limited signal range
  • neuron only operates between a certain range, can only code at one level, we need them to change quickly
47
Q

what is gain control

A
  • gain control is how neurons control their sensitivity
  • how they adpat to new environemenyts
  • adjustement happens over time, get used to environement
48
Q

brain stains - ramon y cajal

A

Brain stains - Ramon y Cajal

brain looked transparent squishiness, stained individual cell bodies and looked at them under a microscope to find that, different but all the same, arranged in clear layers, thickness changes, the brain is organized, function of the cell could be linked to the shape of the cell, common features of neurons across brains.

columns across the cortex has same layers but weight may be different each layer has a number, layer 4 = inputs come in layer 2 = inputs come out

  • Has similar structures (layers, columns) everywhere
49
Q

what did they do with the super computers?

A

hey built this super computer and then thinly diced rat brains and used computer staining techniques to build a 3d model of the rat brain and asses its neuron structure. didnt focus on computations so didnt tell us much about the brain. EU moved money to other neuroscience projects as they realised tehy werent achieving anything.

50
Q

how does visual stimuli get to the brain?

A

retina -. LGN -> cortex

51
Q

what happens in the retina, before LGN?

A
  • detects changes in luminance
  • Luminance: how much light there is somewhere (how many photons)
  • Contrast: how much the light changes across space. it can be described as a decimal (0-1) or as a percentage.
  • Luminance -> Contrast computed with receptive fields
52
Q

what does lgn recieve info about?

A

receiving information about the contrast (NOT LUMINANCE)

53
Q

what happens at the lgn?

A
  • contrast is the currency of the visual system
  • insensitive to lumincance changes, sensitive to changes in contrast
  • if you record from a neuron in the LGN it has two tunings: contrast and eye of origin. this means you can test which eye signal is coming from.
53
Q

signatures of retinal gain control

A
  • Short range
  • “Untuned” (doesn’t care about orientation, direction, size, spatial frequency)
  • Does depend on eye – eyes adapt independently
  • Adjusts the sensitivity of photoreceptor cells (rods and cones) and other retinal neurons to light.
    Helps in adapting to different light intensities, such as moving from a dark environment to a bright one or vice versa.
53
Q

what is the V1?

A

striate cortex, different parts of this area of the brain see different parts of the world, as you more outwards of the cortex different areas of the brain observe different angles of the world. most the V1 is dedicated to the central vision.

53
Q

what has abnormal gain control been found in?

A

Abnormal gain control has been observed or proposed in epilepsy, autism, schizophrenia, Parkinson’s disease as well as normal aging.

but can also be the cause of some neurological diseases

53
Q

signatures of cortical gain control

A
  • Long range
  • Have tuning (e.g. orientation)
  • Complex features (facial expression, blur, gender…)
  • adaptation and local feature contrast
53
Q

what epilepsy may be caused by poor gain control?

A

Photosensitive epilepsy triggered by high-contrast flicker

54
Q

what mutation means youre more likely to get PD

A

LRRK2

54
Q

do both eyes do gain control at the same time?

A

no, they adapt independently

54
Q

what did they do with LRRK2 and fruit flies

A
  • We can take LRRK2-G2019S from humans and insert it into fruit flies.
  • Then the fruit flies get Parkinson’s disease!

stick parkinson gene in fruit fly its in their genome

is there abnormal gain control in the flies?

neurons become way more senitive and active

neurons hyper

respond more quick

tunis - 40% of pd patients carry G2019S

portable eeg scan

measure gain control

less sensiive response function

54
Q

abnormal gain control means

A

your neurons are less sensitive to the environement

55
Q

what is the difference between cortical gain control and retinal gain control?

A

Function: Retinal gain control primarily deals with adapting to different light levels and enhancing contrast at an early stage. Cortical gain control deals with more complex adjustments based on context and higher-level processing.
Mechanisms: Retinal mechanisms include photoreceptor adaptation and lateral inhibition, while cortical mechanisms include normalization, attention modulation, and feedback from higher-order areas.
Role: Retinal gain control provides initial adjustments to ensure signals are within a useful range. Cortical gain control provides sophisticated adjustments for stable and detailed perception.

56
Q

what are the photoreceptors in the retina?

A

cones and rods

57
Q

what is the purpose of lateral inhibition?

A
  • enhances contrast and sharpness of visual signals
  • helps detect patterns and shapes
  • ## prevents us from being overwhelmed y stimuli