vision and proprioception Flashcards
1
Q
what pathway does light take through the eye?
A
- go through cornea
-lense - aqueous humour
- retina at back of eye
2
Q
what does the centre of the retina consist of?
A
- high concentration of photoreceptors
- high visual acuity
- part of fovea
3
Q
what structures are attached to the lease?
A
- ciliary muscle attached via zonular fibres (changes shape to accommodate to image)
4
Q
how is the eye like a camera?
A
- image is inverted but brain flips image
5
Q
diopters
A
- measure lens focussing power = reciprocal of the focal length in metres
- focal length = distance between lens and image
- 1D means focal point is 1m away
6
Q
average human eye diopter strength
A
56-60 diopters
7
Q
refractive indices
A
- outside of eye = 1.00
- cornea = 1.34
- lense = 1.41
- victreous humour = 1.34
8
Q
where does refraction occur?
A
at cornea
refractive index 1.34
48D out of 57D refraction happens here
9
Q
further refraction where
A
lens
means refraction 1.41
10
Q
how is focal length changed?
A
- alter she of Len accommodating by ciliary muscle
- spherical to oval
- motion of lense is called accomodation
11
Q
contraction of ciliary muscle causes what
A
relieves ligamental tension on lens causing lens to squash increasing lens power and shortens local length for closer objects
12
Q
what is myopia?
A
- caused by eye ball being too long or overly powerful cornea
- when someone is nearsighted
13
Q
what is hypermetropia?
A
- opposite of myopia
- far sighter and eyeball too short
14
Q
presbyopia
A
- lens seizes up with age - no longer bulges when ciliary muscle contracts and near -point moves further away
15
Q
the pupil
A
- diameter is first means of adaptation to changing light levels (2-8mm)
- alters amount of light captures x16
- small portion of eyes total light adaptation
16
Q
pupillary muscles
A
- sphincter muscles
- dilator
- as sphincter contract pupil gets smaller and vice versa
17
Q
benefits of smaller pupil
A
- less light reaches retina
- greater depth of field (high quality image)
reduces spherical aberration
reduced glare (scattering of light) - why we can see better in light
- as pupil size reduces it gets closer to a pin hole camera - infinite depth of field (focus)
18
Q
the retina
A
- fovea centralis (high level of visual acuity not very sensitive to light)
- blood vessels
- signal into brain via optic nerve and leave brain via optic disc
19
Q
how does info get from retina to brain?
A
- optic nerve carries info from retina.
- passes through optic disk (ganglion cells) resulting in a blond spot
20
Q
retinal cells
A
- retina transforms image by cone photoreceptors
- other cells types - rods, cones
- bipolar cells, ganglion cells, horizontal and amacrine cells
- once info is transduced within cell needs to be transmitted to ganglion cell forming optic nerve
21
Q
ganglion cells
A
- fire action potentials
- light modulates activity up or down
- takes single to brain
22
Q
cones
A
- don’t have action potential
- modulates membrane potential
- translated via bipolar into change of action potential in ganglion cell
23
Q
what was the structure of the retina
A
- photoreceptors on outside
- light passes through cells structures to reach there’s causing scatter degrading image
- pigment epithelium minimises reflectance and scatter as receptors are adjacent
24
Q
foveal retina
A
- taken cell bodies and pushed them aside for light to do straight through without scattering so centre of eye have higher acuity
- fovea is small bit in middle of eye where cell is teased away for that high visual acuity
25
Q
rods and cone cells
A
- photopigment contained within disks of outer segment
- disks continuously migrate outwards and regenerated
- certain density of these photoreceptors - point spread function - 2 sources of light and shine them onto retina when is system first capable of distinguishing those 2 bits of light
- maximum density is well matched to point spread function
26
Q
what chain of events occur during phototransduction
A
- photopigment bleaching - retinal and opsin combine to make photopigment = rhodopsin (unbleached)
light photon interacts with rhodopsin causing change so becomes bleached - cell membrane hyperpolerised via G-protein as released opsin activates enzyme PDE via G protein, PDE converts to cGMP to GMP opining Na+ channels. closing of the channels causes hyper polarisation of cells as K+ continues to leak out
- neural output of ganglion cell modified - rod/cone hyper-polarisation results in less neurotransmitter release and modulates membrane potential of bipolar and modulates firing rate of ganglion cell
27
Q
increased light can what
A
increase or decrease fire depending on ganglion cells being excitatory or inhibitory
about modulating cells
28
Q
visible range of luminance
A
- human vision functions across 10 to power of 15 units of luminance
29
Q
scotopic v photopic vision
A
- different photoreceptors and different light levels
- low light = rods as highly sensitive but low acuity (scotopic)
- brighter light = cones only as low sensitivity and high acuity (photopic) on sunny day rod cells are completely bleached
30
Q
photopic vision
A
- high luminance
- cones only
low sensitivity and high acuity - fovea land peripheral
31
Q
scotopic vision
A
- low light vision
- rods only
- high sensitivity and low acuity
- non-foveal
32
Q
mesopic vision
A
- intermediate luminance (dusk)
- rods and cones
- intermediate sensitivity and acuity
- foveal and peripheral
33
Q
what 4 mechanisms adapt to luminance
A
- pupil size (takes a few seconds)
- switch of photoreceptors rods and cones (few seconds)
- dark adaptation (bleaching and regeneration of photopigment. takes 15-20 mins to adapt visually)
- field adaptation (light adaptation - cellular process in photoreceptors. instantaneous adaptation)
34
Q
rods vs cones
A
- rods more sensitive than cones
- bigger convergence in sensitivity (high convergence of rods onto ganglion cells)
- convergence can be altered in different light
- mesopic conditions rods and cones could converge together
35
Q
how many of each photoreceptors converge onto ganglion cells?
A
1 cone = 1 ganglion cell
75,000 rods = 1 ganglion cell
36
Q
what is the distribution of rods and cones in the retina?
A
- foveal vison = cone dependant
- deviate from fovea - increase of rod cells
- high density of both in centre
37
Q
dark adaptation - bleaching
A
- sunlight > pitch black room = regeneration of cones and then rods will continue to regenerate until fully done
38
Q
what processing happens between photoreceptor and ganglion cell
A
- 130mill photoreceptors in eye - not all info to brain - retina interested in spatial and temporal changes - processes photoreceptor output to identify the changes and send that info to brain through cells (horizontals and amocrines)
39
Q
how do we detect postal change
A
- detect edges
- retina detects edges sends that info and loses the rest
40
Q
how does the retina send spatial (edges) info to brain?
A
- receptive field of ganglion cell = area of retina which activates that cell
- ganglion cell is the final output of retina, each cell respond to many photoreceptors so shine light on retina to determine ganglion receptive field
41
Q
what is lateral inhibition
A
- the capacity of an excited neuron to reduce activity of its neighbours
- mediated by horizontal cells
- stripe of light best activates ganglion cell - excitatory cells in middle and inhibitory in periphery - light stripe activate so responds to edge (central exiting and lateral inhibiting)
42
Q
how does lateral inhibition create contrast illusions?
A
- terrible of detecting absolute levels of light
- surroundings affects acitivity of cell due to retina
43
Q
types of cone cell in colour vision
A
- red
- green
- blue
44
Q
why do we have 3 types of cone
A
- responds to stimulus intensity
- if intensity doesn’t change = green
- a monochrome system doesn’t allow you to distinguish between different light levels
45
Q
what type of system does our colour vision have?
A
- 3 channel system
- red, green and blue
46
Q
explain the colour triangle of the 3 channels
A
- any colour can be dialled up by combination of red green and blue
- cannot distinguish certain green wavelengths
47
Q
how can we define colour
A
- saturation = strength, pure red fully saturated and white is fully unsaturated
- hue - colour itself
- no wavelength can stimulate green cones without red or blue cones
48
Q
explain the neural process of colour (colour opponent)
A
- takes place in retina
2, ganglion cells don’t respond to red, green or red alone but a combination - 3 channels hitting ganglion cell and it responds best to certain combos
4.
49
Q
colour opponent
A
- 3 opponent channels in retinal output
- May explain why yellow is perceived to be a primary colour
- Explain impossible colours – can have bluish-green (turquoise) but not yellowish-blue or reddish-green
50
Q
colour constancy
A
- Colours tend to look the same despite large changes in wavelength of illuminating light
- Multiple mechanisms – one is adaptation we discussed previously
- High stimulated colour channels will tend to adapt and become less responsive
51
Q
how does colour blindness work?
A
- deuteranope
- lost green receptor
- accept pair of colours as match as long as they have same R and B components
52
Q
colour blindness - rarest
A
- monochromats = only see black and white
- dichromats = lost your blue channel
53
Q
define proprioception
A
- the sense of the relative position of neighbouring parts of the body
- muscle spindles and Golgi tendon organs
54
Q
how do you get a sense of where your limb is
A
- joint capsule receptors = Ruffini, paciniform, golgi-type and free nerve endings (historical)
- modern shows minimal role of joint capsule
55
Q
what does a muscle spindle consist of?
A
- bindle of thin muscle fibres contained within capsule
- parallel with main extrafusal muscle but generates no useful force
- wrapped round air of sensory axons detecting muscle stretch
- gamma motor neurons cause active contraction of spindle
56
Q
what do muscle spindles detect?
A
- static length of muscle
- rate of change of muscle stretch (velocity)
57
Q
characteristics of muscle spindles
A
- Joint angles calculated from changes in muscle length signalled by spindles
- Central part of muscle spindle is non-contractile
- Stretch-sensitive ion channels in sensory axons are activated when muscle is stretched
- 400 spindles in soleus muscle
- Primary endings: signal position and velocity. Transmitted via 1a afferents. Sensitive to vibration
- Secondary endings: position only, via group II afferents
- Gamma fibres: contractile element of spindle. No useful force output – purely intended to keep spindle taught
58
Q
how does alpha-gamma coactiviation maintain muscle spindle sensitivity?
A
- 1a spindle afferent fires signal muscle length
- contraction of main muscle cause slackened spindle
- causes drop of firing rate and loss of sensitivty
- gamma active`tion contracts spindle maintaining sensitivity
59
Q
2 pieces of evidence that support the role of spindles for sensation
A
- muscle vibration - 80-100Hz of vibration activates 1a afferents producing muscle stretch illusion
- muscle conditioning effects - prior muscle stretch/ condition significantly affects joint position sense due to muscle becoming slack affecting spindle output
60
Q
Golgi tendon organ and proprioception
A
- contributes to joint rotation sense (signals force and heaviness)
- important when muscle movement is ambiguous
- between muscle and tendon
- when stretched, 1b afferent axon is compressed by collagen fibres so rate of firing increases
