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Neurophysiology > Visual system- retina to cortex > Flashcards

Visual system- retina to cortex Flashcards

1
Q

What are horizontal and amacrine cells thought to be involved in

A

Setting up centre-surround visual fields, enabling lateral inhibition to provide greater contrast

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2
Q

What allows high acuity in the fovea for cones

A

Often a 1:1 relatinoship between cones/bipolar cells/ganglion cells meaning low convergence, small receptive fields, densely packed

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3
Q

What is sacrificed for high acuity in cones at the fovea

A

Sensitivity

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4
Q

What reduces acuity but improves sensitivity at the peripheral retina for cones

A

More convergence of cone info -> bipolar cell info -> ganglion cell info

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5
Q

Why does it make sense for our cone periphery to be high sensitivity but low acuity

A

It is more important our periphery is sensitiive so we can notice things, then turn and use our foveally dominated vision for detail

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6
Q

How sensitive vs high acuity are the rods

A

Low acuity, very high sensitivity

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7
Q

Why is rod vision low acuity but high sensitivity

A

Info from many rods converges onto a single rod bipolar, which is compressed again by ganglion cells

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8
Q

Why does convergence reduce acuity

A

The brain doesn’t know which one of the 15-30 rods that connect to each bipolar cell the signal came from before they were all pooled

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9
Q

Sensitivity and accuracy of scotopic vs photopic vision

A

Scotopic vision- very sensitive, not very accurate

Photopic vision- very accurate, not very sensitive

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10
Q

How do amacrine cells affect rod vision during mesopic conditions

A

Amacrines link rod and cone pathways via gap junctions, so the rod signals can piggyback onto the cone bipolar pathways to provide add info to the cone pathway to make it more sensitive (Wassle et al, 1995)

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11
Q

What are amacrine cells sometimes called for their role in mesopic vision

A

Piggyback cells

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12
Q

What is the result of the ganglion cells receiving a mix of info from rods and cones in mesopic conditions

A

Vision has a balance between acuity and sensitivity

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13
Q

What is the pathway taken by info in mesopic conditions in the retina

A

Rods ->Rod bipolars -> All amacrine cells -> Cone bipolars -> Ganglion cell

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14
Q

What conformational change marks the start of phototransduction

A

Photons induce a confirmational change in retinal (cis retinal -> trans retinal), which activates the opsin (a GPCR) that activates the G protein transducin

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15
Q

What is the opsin in rods

A

Rhodopsin

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16
Q

What are the opsins in cones

A

Photopsins- 3 types; red, green, blue

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17
Q

What is the effect of the activation of G protein transducin in phototransduction

A

Transducin triggers phosphodiesterase (PDE) to hydrolyse cGMP, reducing cGMP levels which closes cGMP-gated channels

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18
Q

What is the effect of cGMP-gated channels closing in phototransduction

A

The photoreceptor hyperpolarises in a graded manner, as Na+ can no longer enter through the channel

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19
Q

What is the result of graded hyperpolarisation of photoreceptors due to phototransduction

A

Corresponding graded reduction in the rate of neurotransmitter release onto bipolar cells

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20
Q

When taking intracellular recordings from a single cone cell from a turtle retina stimulated with increasing amount s of light- what is the effect of light

A

Light hyperpolarises the cone, at the highest light levels the response is saturated and the receptor is said to be bleached

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21
Q

What is the sensitivity to bleaching of rods vs cones

A

Rods- more sensitive, bleach at ambient light levels meaning they don’t function in daylight
Cones- less sensitive, are fully active even in bright sunshine

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22
Q

What 4 mechanisms terminate the phototransduction cascade

A

Inactivation of rhodopsin, inactivation of transducin, inactivation of phosphodiesterase (PDE), activation of guanylate cyclase

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23
Q

Phototransduction cascade termination- what causes inactivation of rhodopsin

A

Rhodopsin is phosphorylated by the opsin kinase, then arrestin binds to phosphorylated rhodopsin, completely deactivating it- resuming dark current

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24
Q

What happens to rhodopsin in the dark

A

Rhodopsin regenerates after being bleached

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25
Q

What underlying intracellular factor drives termination of the phototransduction cascade

A

Low intracellular Ca2+ levels caused by closing of cGMP-gated channels by high light levels

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26
Q

What is the purpose of termination of the phototransduction cascade

A

Allows light adaption of the bleached photoreceptor, so membrane can be gradually depolarised to about -35mV again and we can see again

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27
Q

Phototransduction cascade termination- what causes inactivation of transducin

A

Occurs through the hydrolysis of bound GTP to GDP, via an intrinsic GTPase activity

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28
Q

Phototransduction cascade termination- what causes inactivation of phosphodiesterase (PDE)

A

The inactivation of transducin causes it to dissociate from PDE, resulting in a cessation of PDE-mediated cGMP hydrolysis

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29
Q

Phototransduction cascade termination- what causes activation of guanlyate cyclase

A

Guanylate cyclase is activated by gualynate cyclase activating protein (GCAP), restoring cGMP levels and promoting the reopening of cGMP-gated channels

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30
Q

What 2 types of bipolar cell receptive field are there

A

ON-centre, OFF-centre

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31
Q

What maximally excites an ON centre bipolar cell

A

Light in the centre of the receptive field, dark in the surround

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32
Q

What maximally excites an OFF centre bipolar cell

A

Dark in the centre of the receptive field, light in the surround

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33
Q

What do bipolar cells respond to rather than light an why

A

Local contract, as they receive opposing input from surruonding receptors

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34
Q

Why does it make sense for bipolar cells to respond to contrast rather than light

A

We are interested in seeing edges andnot uniform illumination or darkness

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35
Q

Who is credited with discovering centre-surround receptors

A

Kuffler (1953)

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36
Q

How do the centre-surround receptive fields of bipolar cells allow lateral inhibition

A

eg ON-centre bipolar cells, the antagonistic surround opposes the responses in the receptive field centre
Bipolar cells thus have opposing input from surrounding receptors and respond to local contrast- lateral inhibitiion

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37
Q

What is the physiology behind the lateral inhibition of eg ON-centre bipolar cells

A

Horizontal cells make connections with centre photoreceptors as well as lateral antagonistic GABAergic connections with surround receptors, (that cause IPSPs), allowing them to influence surrounding photoreceptors and bipolar cells

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38
Q

What would be the result of uniform light on the ON-centre or OFF-centre bipolar cell receptive field

A

No net response, as activation of the centre/surround will cancel out the surround/centre

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39
Q

Study showing the effectof light presented in different parts of the bipolar cell receptive fields

A

Werblin and Dowling (1969)- eg with an ON bipolar cell, activity was high when light was shone on the centre, then dropped when light was also shone on the annulus
OFF cell showed opposite response

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40
Q

What dictates whether a bipolar cell is ON or OFF centre

A

OFF and ON bipolar cells express different glutamate receptors on their dendrites

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41
Q

What glutamate receptors are expressed in OFF vs ON bipolar cells

A

OFF- AMPA

ON- mGluR6

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42
Q

Response of OFF bipolar cell to glutamate

A

When glutamate binds to AMPA it opens a cation channel -> Na+ enters causing depolarisation and NT release onto ganglion cell
Thus, is excited in the dark

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43
Q

Response of ON bipolar cell to glutamate

A

When glutamate binds to mGluR6, it closes a cation channel -> hyperpolarisation and no NT release onto ganglion cell
Thus, is not excited in the dark

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44
Q

Study showing effect of inactivatnig ON-centre bipolar cells in monkeys- procedure

A

Schiller et al (1986)- pharmacologically inactivated ON centre bipolar cells in monkeys, using blocker amino phosphonobutyrate (ABP)

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45
Q

Study showing effect of inactivatnig ON-centre bipolar cells in monkeys- results

A

The animals showed a deficit in their ability to detect stimuli that were brighter than the background, but could still see objects that were darker than the background
Suggests OFF and ON pathways are seperate an parallel

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46
Q

What are ON bipolars also called

A

Invaginating cone bipolars

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47
Q

What are OFF bipolars also called

A

Flat cone bipolars

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48
Q

How do the connectinos between bipolar cells and ganglion cells differ

A

The dendrites of OFF ganglion cells synapse with OFF bipolar cells deeper in the inner plexiform layer (closer to receptors)
Dendrites of ON ganglion cells synapse with ON bipolar cells at a more shallow level

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49
Q

When is the max response of ON centre retinal ganglion cells

A

Max response when light in the centre, and dark in the surround

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50
Q

When is the max response of OFF centre retinal ganglion cells

A

Max response when darkness in the centre and light in the surruond

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51
Q

How do both ON and OFF retinal ganglion cells response to luminance contrast (either from light in centre/dark surround or vv)

A

Increased firing patterns

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52
Q

What is an OFF centre RGC doing when an ONcentre RGC is firing at its highest level

A

OFF centre RGC is completely silent

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53
Q

Response of RGCs to a light/dark edge- what is the response of an OFF centre ganglion cell to dark in the centre vs surround generally

A

OFF-centre RGC- dark in the centre causes depolarisation, dark in the surround causes hyperpolarisation

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54
Q

Response of OFF RGCs to a light/dark edge- no stimulation of receptor field

A

Weak basal level of signsl

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55
Q

Response of OFF RGCs to a light/dark edge- edge of dark light enters surround only (only edge of surround is dark)

A

Hyperpolarisation, reduction in signal

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56
Q

Response of OFF RGCs to a light/dark edge- edge of dark light starts to include the centre

A

Partial inhibition by darkness in surrouns is overcome, APs increased due to depolarisation of centre

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57
Q

Response of OFF RGCs to a light/dark edge- dark light fills whole surround

A

Depolarising dark centre response is cancelled out by the hyperpolarising surround response

58
Q

How is info about increases and decreases in luminance carried to the brain

A

By axons of 2 seperate bipolar and RGC types in parallel pathways

59
Q

What do RGC cells respond to just like bipolar cells

A

Edges/contrast- light regions stimulation ON ganglion cells and dark regions simulate OFF ganglion cells

60
Q

What are the 5 main types of RGC

A

P type, M type, non M non P, photosensitive ganglion cells, ganglion cells projecting to superior colliculus

61
Q

Which one of the 5 main RGC types are not invovled in perceptual vision

A

Photosensitive ganglion cells

62
Q

What is the proportion of the different types of RGC

A

90% parvocellular
5% magnocellular
5% koniocellular

63
Q

What are P type RGCs

A

Parvocellular cells, historically called midget cells due to small dendritic tree

64
Q

What are M type RGCs

A

Magnocellular cells, historically called parasol cell due to extensive dendritic tree

65
Q

What are non M non P type cells

A

Koniocellular cells, less well characterised, many subtypes

66
Q

What do photosensitive ganglion cells contain

A

Photopigment melanopsin

67
Q

Where do photosensitive ganglion cells project

A

Project to SCN via the retinohypothalamic tract, invovled in setting and maintaining circadian rhythms
Project to LGN connecting with the Edinger-Westphal nucleus for control of pupillary light reflex

68
Q

What do ganglion cells projecting to the superior colliculus have a role in

A

Saccadic eye movement

69
Q

Receptive field size for P cells vs M cells

A

P cells- much smaller receptive fields, can discern detail

M cells- larger receptive fields

70
Q

Speed of conduction for P cells vs M cells

A

P cell axons conduct impulses much more slowly than M cells

71
Q

Sustained vs transience of response of P cells vs M cells

A

P cell responses, especially to colour, can be sustained

Responses of M cells are much more transient

72
Q

Response to colour and contrast of P cells vs M cells

A

P cells- sensitive to colour, require high contrast stimuli

M cells- not sensitive to colour, more sensitive to low-contrast, black and white stimuli

73
Q

What are the distinct functional properties of M and P type cells the start of

A

Parallel processing in the visual system

74
Q

Function of M type cells

A

Highly sensitive to low-contrast stimuli and rapid movement visual signals

75
Q

Function of P type cells

A

Detection of visual signals relating to fine details and high contrast, relatively insensitive to low contrast stimuli and rapid movement visual signals

76
Q

Do the M cells mean humans have motion sensitive RGCs?

A

No- the M cells feed into the motion pathway at HIGHER levels of the visual pathway (Bach, 2000)

77
Q

What can the receptive fields of P type ganglion cells show due to their sensitivity to colour

A

Red/green colour opponency

78
Q

What are the 4 types of centre-surround receptive fields of P type cells

A

Green-centre ON/red centre OFF
Green centre OFF/red centre ON
(and vv w red centre)

79
Q

What can the receptive fields of non M/non P type ganglion cells show

A

Blue/yellow colour opponancy

80
Q

What creates yellow in blue/yellow opponancy in non M/non P ganglion cells

A

Combination of red and green cones

81
Q

Who discovered the morphology of the blue ON/yellow OFF ganglion cell

A

Dacey and Lee (1994) via intracellular recordings and staining of these ganglion cells in monkey retina

82
Q

What types of blue/yellow opponency cells are there

A

Blue ON/yellow OFF cell- gives ON respones to blue light stimulation and OFF responses to yellow (coextensive receptive fields)
Blue OFF yellow ON cells rarely observed

83
Q

What does SCN stand for

A

Suprachiasmatic nucleus

84
Q

How are individual cones entirely colour blind

A

Response of a cone is a reflectino of captured photons regardless of wavelength- the wavelengths detected by the different cones all overlap, so any colour is likely to activate the simultaneously

85
Q

What is the consequence of individual cones being entirely colour blind

A

It is impossible to determine whether a change in membrane potential of a cone is from exposure to many photons at relatively insensitive wavelengths, or fewer photons at wavelengths the cone is most sensitive to

86
Q

How is the ambiguity of discriminating colours based on photoreceptor activity resolved

A

Opponent mechamisms- comparing the activity in different classes of cones at the same point in time to extract colour info from stimuli

87
Q

What are the 3 opponent mechanisms used in discriminating colours

A

Comparing difference between R and G cones, B and (R+G->Y) cones, achromatic mechanisms for detecting differences in luminance/contrast

88
Q

How would a red ON centre/green OFF surround P ganglion cell respond to- red light on centre

A

Red cones in centre are activated, leading to RGC depolarisation and increased activity

89
Q

How would a red ON centre/green OFF surround P ganglion cell respond to- overall red light

A

Evokes response, but response is reduced because some of the red light will stimulate the green cones that feed into the inhibitory surround,but not enough to cause full cancellation

90
Q

How would a red ON centre/green OFF surround P ganglion cell respond to- red light in centre, green light in surround

A

No response- depolarising response to red light in centre is cancelled by the hyperpolarising response to green light in the surround

91
Q

What is the most common form of colour blindness and how is it linked

A

Red-green colour blindness is sex-linked

92
Q

Why were colour blind people useful in WW2

A

Colour blind people were better at detecting camoflague as they could pick up differences between greens/browns/yellows that people who saw a normal spectrum of colours couldn’t

93
Q

What can red/green opponent P ganglion cells respond to other than colour

A

Responses of red and green cones are used to detect luminance changes, providing fine detail of P pathway while being achromatic

94
Q

How can red/green opponent P ganglion cells respond to luminance changes

A

White light contains all the spectrum of colours, so will include some red and green wavelength light

95
Q

What are M type ganglion cells called in terms of their receptive fields

A

Broad band cells

96
Q

Why are M type ganglion cells called broad band cells

A

Large receptive fields, get combined input from red and green cones in both the centre and surround

97
Q

What are the 2 types of M type ganglion cells

A

Red and green ON centre/ red and green OFF surround

Red and green OFF centre/red and green ON surround

98
Q

What do M type ganglion cells measure and why

A

Can only measure brightness contrast as they are colourblind because they have both R and G cones in both centre and surround

99
Q

What is the structure of amacrine cells

A

Lack axons, large dendritic trees, different types connect to different bipolar cells and/or ganglion cells

100
Q

Are most amacrine cells inhibitory or excitatory

A

Most are inhibitory using GABA, glycine or dopamine

101
Q

How do amacrine cells respond to illumination compared to bipolar cells

A

Amacrine cells respond transiently to illumination giving ON-OFF responses, compared to the sustained response of bipolar cells

102
Q

Who showed how ganglion cell responses are built from the interactions of horizontal and bipolar cells

A

Dowling and Werblin (1970s)

103
Q

Where are synapses between photoreceptors and bipolar/horizontal cells located

A

In the outer plexiform layer

104
Q

How many photoreceptors do bipolar cells receive input from in the central fovea vs peripheral retina

A

Bipolar cells receive input from a cluster of photoreceptors ranging from 1 (in central fovea) to thousands (in peripheral retina)

105
Q

How do the horizontal and amacrine cells differ in their location of function

A

The lateral connections of amacrine cells integrate bipolar input to ganglion receptive fields, while horizontal cells provide photoreceptor input to bipolar cells

106
Q

What phenomenon supports the existence of photosensitive retinal ganglion cells

A

Mutant mice lacking rods and cones can still synchronise their sleeping and waking with the rise and setting of the sun despite behaving totally blind

107
Q

How do photosensitive retinal ganglion cells differ to photoreceptors

A

Photosensitive retinal ganglion cells depolarise to light, have very large receptive dendritic fields, and there is only a few thousand

108
Q

What are the only source of retinal output through the optic nerve

A

The ganglion cells

109
Q

How are ganglion cells different to all other retinal cells in their electrical transmission

A

Ganglion cells are the only retinal neurons that fire APs- all other retinal cells de/hyperpolarise with a rate of neurotransmtiter release proportional to the membrane potential

110
Q

What form of organisation does the retina have

A

Laminar organisation, cells are organised in layers

111
Q

What is contained in the outer segment of photoreceptors

A

A stack of membranous disks with light sensitive photopigments in their membranes that absorb light

112
Q

How does the structure of rods and cones differ

A

Rods- long cylindrical outer segment containing many disks

Cones- shorter, tapering outer segment with fewer membranous disks

113
Q

Why are rods over 1000x more sensitive to light than cones

A

Due to the higher no of disks and higher photopigment conc in rods, plus rods amplify the response to light more than cones

114
Q

What is a consequence for colour perception of the lower no of cones in our peripheral retina

A

We are poorer at discriminating colours on our peripheral retina

115
Q

How do we see colour at night

A

We cannot perceive colour differences at night when cones are not active- the peak sensitivity of rods is about 500nm, so in scotopic light levels objects tend to look dark blue-green

116
Q

What is the dark current

A

The steady influx of Na+ through cGMP gated channels in the photoreceptors that keeps the membrane potential at about -30mV IN THE DARK

117
Q

What is rhodopsin’s structure

A

Consists of receptor protein opsin, and prebound agonist retinal

118
Q

Why is the confirmatinoal change in retinal, activating opsin, called bleaching

A

It changes the wavelengths absorbed by the rhodopsin as the photopigment turns from purple to yellow

119
Q

How does the biochemical cascade in phototransduction make our visual system very sensitive to light

A

Signal amplification- each photopigment molecule activates many G proteins, and each PDE enzymes breaks down many cGMPS molecules

120
Q

What causes the rods to not work in bright light

A

cGMP levels in rods fall to the point the response to light becomes saturated- increasing light causes no additional hyperpolarisation as all the cGMP gated Na+ channels have already closed

121
Q

How does phototrasnductin differ in cones and rods

A

Cones have different opsins in their membraneous disks

122
Q

What are the 3 different opsins cones can contain

A

Short wavelength ‘blue’ cones, medium mavelength ‘green’ cones, long wavelength ‘red’ cones

123
Q

Preferred wavelength of blue cones

A

430nm

124
Q

Preferred wavelength of green cones

A

530nm

125
Q

Preferred wavelength of red cones

A

560nm

126
Q

What determines colour perception

A

The relative contributions of short medium and long wavelength cones to the retinal signal

127
Q

Who proposed the 3 cone type idea first

A

Young (1802) showed all colours of the rainbow could be greater by mixing the proper ratio of G R and B light, proposing 3 receptor types each sensitive to a diffeent wavelength spectrum

128
Q

What is the dominant theory of colour vision cauued

A

Young-Helmholtz trichromacy theory

129
Q

What causes colourblindness

A

One or more cone photopigment types is missing

130
Q

What is achromatopsia

A

Lack of colour vision

131
Q

Study showing example of achromatopsia

A

On the Micronesian island of Pingelap, more than 5-10% of the population is colourblind, due to a genetic mutation associated with incomplete cone development

132
Q

What happens in dark adaption

A

Over minutes-hour, all-cone daytime vision transitions to all-rod nighttime vision, with light sensitivity increasing a millionfold in this period

133
Q

What does the pupil do to allow dark adaption

A

Pupils dilate allowing more light to enter the eye, but this only increases light sensitivity by a factor of about 10

134
Q

What is the main cause of dark adaption

A

Regeneration of unbleached rhodopsin and an adjustment of the functional circuitry of the retina so info from more rods is avaiable to each ganglion cell

135
Q

What happens when a dark adapted eye goes back into bright light

A

It is more sensitive, so is temporarily saturated- over 5-10 mins, the eyes undergo light adaption to reverse the changes in the retina that accompanied dark adaption

136
Q

What happens to membrane potential in the process of light adaption

A

When we step out into bright light after being in the dark, the cones are maximally hyperpolarised meaning we cannot see further changes in light level- gradual depolarisation of the membrane allows us to see again

137
Q

What is Ca2+ doing when the cones are in the dark

A

Ca2+ enters the cones through cGMP-gated Na+ channels, and inhibits guanylyl cyclase that synthesises cGMP

138
Q

How does Ca2+ allow light adaption when we step into bright light

A

cGMP-gated channels close in bright light, curtailing the flow of Ca2+ into the photoreceptor alongside Na2, meaning more cGMP is synthesised as Ca2+ can’t inhibit guanyly cyclase, and the cGMP channels open again

139
Q

How is the membrane able to be gradually depolarised again in light adaption

A

Ca2+ allows cGMP channels to open again via a cascade, despite light level not changing

140
Q

What is the purpose of light and dark adaption

A

Ensures photoreceptors are always able to register relative changes in light level, though info about the absolute level is lost

Neurophysiology (23 decks)

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