Retina Night and Day - Week 5 Flashcards

1
Q

Over what dynamic range can your visual system detect changes in light level?

A

A dynamic range of about 10 log units

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2
Q

T/F: a bright flash of light prevents detecting change of light level

A

False. Even with a bright light flashed in your face, you can still detect changes in light levels

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3
Q

What rate/amount of photons should fall on the photoreceptors to be able to detect a change in light level?

A

The amount of photons must be more than the rate of thermal/accidental isomerisation of rhodopsin

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4
Q

Is light needed for rhodopsin to convert into metarhodopsin?

A

No. Not always. occasionally rhodopsin can isomerize without light

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5
Q

When looking at a faint star, what governs your ability to see it?

A

The probability that the photons of light hit the retina. This is governed by a poisson distribution

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6
Q

What factors influence how efficiently light can get to the back of your eye and hit the retina? (2)

A
  1. Pupil size

2. How the light gets converted into a chemical signal

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7
Q

Why does the visual system become less sensitive to light in higher light levels

A

It’s trying to avoid saturation

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8
Q

What suggests we have 2 processes for our visual system (duplex retina)?

A

The characteristic “break” in sensitivity found in light and dark adaptation

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9
Q

How does retinal eccentricity affect the rod branch in dark adaptation?

A

Rod branch occurs earlier (and is more sensitive) with increased eccentricity

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10
Q

Where are cones most dense? Are rods present here?

A

Cones are most dense at the fovea. No rods are here

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11
Q

Where is rod density highest?

A

15 degrees from the fovea

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12
Q

What would the dark adaptation curve look like at the fovea?

A

Cone branch followed by flat horizontal line of cone branch. That’s it

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13
Q

How do the following influence the size of the rod-cone break in dark adaptation:

  • spot size
  • blueness of spot
  • eccentricity of spot
A

Spot size: increase in spot size will increase the break
Blue colour: will increase break (because short wavelengths give more break, vice-versa for long)
Eccentricity: More break at 15 degrees from retina

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14
Q

Why is phototransduction in rods slower than in cones?

A

In rods, the phototransduction proteins are inside transmembrane discs enclosed within the outer segment of the membrane.
– Therefore, they are in a different location than the channels

(This is not a problem with cones as the membrane is continuous therefore the photransduction proteins and the channels that need to be closed are in the same place)

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15
Q

Compare the general shapes of rods vs cones. How does this affect directional sensitivity?

A

Rods: Square shape
Cones: Conical shape, which acts as a waveguide

Conical shape results in greater directional sensitivity

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16
Q

Which visual system is incapable of saturation?

A

Cone system

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17
Q

List 6 factors that can influence dark adaptation:

A
  • spot size
  • location/eccentricity of stimulus
  • speed or duration of stimulus
  • colour/wavelength of stimulus
  • background intensity
  • amount of bleaching
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18
Q

Which visual system is faster at recovering from a bright flash? Rods or Cones?

A

Cones recover about 5 to 10 times faster

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19
Q

By how much are rods more sensitive than cones?

A

about 2 log units more sensitive

20
Q

How does the visual system increase its dynamic range of detection?

A

Duplex retina

21
Q

How do the rod and cone pathways interact?

A

Rod system patches onto the cone system

Rods attach to on-bipolar cells and then patch via A2 amacrine cells into the on and off cone bipolar cells (that are inactive at low light levels)

22
Q

Where do bipolar cells synapse?

A

Inner plexiform layer

23
Q

Do rod bipolar cells directly contact ganglion cells?

A

No

24
Q

Describe how the rod pathway provides an excitatory signal to ON-ganglion cells:

A

AII amacrine cell talks to ON-cone bipolar cell via GAP JUNCTIONS

  1. About 15 rods converge onto one rod bipolar cell
  2. Rod bipolar cell synapses in IPL with A2 amacrine cell
  3. A2 amacrine cell talks via gap junctions to on-cone bipolar cells
  4. On-cone bipolar cell provides excitatory signal to on-ganglion cell
25
Q

How do rods provide a signal to OFF-ganglion cells?

A

via AII amacrine cells talking to OFF-cone bipolar cell via inhibitory synapses

26
Q

Describe the two ways that amacrine can contact a bipolar cell:

A
  1. via gap junctions with on-cone bipolar cells (electrical synapses)
  2. via inhibitory glycernergic synapses with off-cone bipolar cells (chemical synapse; glycine/GABA)
27
Q

Light hyperpolarises photoreceptors, but what about bipolar cells?

A

Bipolar cells get depolarised (it’s a sign conversing synapse)

28
Q

Is Glycine an inhibitory or excitatory neurotransmitter

A

Inhibitory

29
Q

How do horizontal cells interact with photoreceptors

A

Horizontal cells receive excitatory input from the cones (when depolarised and releasing neurotransmitter) and send inhibitory feedback in return.

30
Q

Describe the convergence of rods to ganglion cells

A

1500 rods to 100 rod-bipolar cells to 5 AII amacrine cells to 4 cone-bipolar cells to 1 rGC

31
Q

Describe the convergence of cones to ganglion cells

A

16 cones to 4 cone-bipolar cells to 1 rGC

32
Q

How do AII amacrine cells modulate the rod-bipolar cell signal?

A

Signal gain (signal is amplifed by at least one log unit)

i.e. amacrine response at least one log unit more sensitive than rod-bipolar

33
Q

How does the rod photoreceptor response change with a brighter background?

A

With brighter background:

  • responses become smaller
  • responses become faster
  • intensity-response function shifted to brighter light levels
34
Q

In what 2 ways can we amplify our photoreceptor signal?

A
  1. phototransduction cascade [the 2 amplification steps]

2. AII amacrine cells

35
Q

How does a low level of calcium influence light adaptation?

A

Response to short flash = prolonged

Response to prolonged flash = slower, larger, and no recovery

36
Q

Steps of phototransduction:

A
  1. initial dark current, most cGMP channels open
  2. Photons captured by rhodopsin; converts to MII (via 11cis to all-trans)
  3. MII binds many transducin [amplification step]
  4. alpha transducin converts GDP to GTP; binds + activates PDE
  5. PDE hydrolyse cGMP to GMP [amplification step]
  6. reduced cGMP; channels close
  7. Influx of cations into outer segment
  8. Hyperpolarisation
  9. End of dark current: stop glutamate release
  10. De-activation
37
Q

How does low calcium level influence phototransduction?

A

Low calcium causes activation of GC (guanylate cyclase), which converts GTP to cGMP

More cGMP means cationic channels re-open

38
Q

What is the level of calcium caused by:
Bright background
Dim background

A

Bright: results in low calcium
Dim: high calcium

39
Q

Describe the activity of Guanylate Cyclase in a dim background

A

GCIP is activated and inhibits GC. GC response decreases

40
Q

Describe the concentration of inactive opsin in bright vs dark conditions

A

Bright: Low conc. inactive opsin
Dim: High conc. inactive opsin

41
Q

True/False: Receptor adaptation is solely responsible for light adaptation

A

False. Receptor adaptation only partly accounts for light adaptation

42
Q

how do the following affect bipolar cell and GC cell responses:
Dim background
Bright background

A

Dim: bipolar unchanged, GC decreased
Bright: bipolar decreased, GC decreased

43
Q

In bright background, which response changes more? Cone or GC (guanylate cyclase)?

A

Guanylate cyclase decreases more than cone

44
Q

Where does signal gain occur?

A

At the post-receptoral level

45
Q

Which has better temporal resolution, rods or cones?

A

Cones