Retina & Fovea Specialisations Flashcards

1
Q

What is the retina?

Where does it terminate?

What is it’s outer boundary?

What does the inner surface of the retina touch?

A
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2
Q

How many layers of the retina are there?

A

10 (lowkey you should know them)

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3
Q

What is the external limiting membrane of the retina formed by?

A

Formed by tongue junctions between Muller cell processes and the photoreceptor cells.

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4
Q

What exists in the outer nuclear layer of the retina?

A

The nuclei of the photoreceptors ( so the nuclei of rods and cones).

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5
Q

What exists in the outer plexiform layer of the retina?

A

Muller cell processes and photoreceptor axons

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6
Q

What exists in the inner nuclei layer of the retina?

A

Nuclei of your; bipolar cells, amacrine cells and horizontal cells.

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7
Q

What exists in the inner plexiform layer of cells?

A

Synapses between bipolar and ganglion cells

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8
Q

What exists in the ganglion layer of the retina?

A

Ganglion cell nuclei.

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9
Q

What exists in the nerve fibre layer of the retina?

A

Axons that have projected out of the ganglion cells which run back towards the optic nerve.

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10
Q

What is the inner limiting membrane of the retina?

A

Junction between the retina and the vitreous. It is formed primarily by muller cell end feet

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11
Q

Where does the retina get it’s blood supply from?

A
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12
Q

Describe how the opthalmic artery goes on to supply blood to your eye.

A
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13
Q

What are the 2 types of photoreceptors?

Describe what they are specialised for?

Describe their structure.

A

They both have outer segments containing discs which contain visual pigments.

Inner segments are packed full of mitochondria and other cell organelles.

Then obviously both have a soma and axon.

Then the terminal on a rod is called a Spherule and the terminal on a cone is called a pedicle

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14
Q

What are visual pigments?

What are they made of?

What remains the same in all four visual pigments?

What therefore chnages in each visual pigment?

A

They are chroma-proteins.

They contain a chromophore and a protein element.

Chromophore is the same in all four visual pigments. It is retinal.

The proetin (opsin) - this is what determines the spectral nature of each visual pigment.

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15
Q

What is photoisomerisation and how does this occur in the visual pigment?

What is visual pigment bleaching?

A

When a photon of light is used to change the structure of a structure.

So basically in it’s natural resting form, the chromophore in the chromaproetin (visual pigment) is bent. When it absorbs a photon it suddenly straightens out (looses that kink). This is called Photoisomerisation.

[Goes from 11-cis retinal to all trans retinal]

Photoisomerisation is the first event that triggers the indction of a signal through the phtoreceptor. (Basically its the thing that starts everything up).

Suddenly because the chromophore part (retinal) has starightened out it no longer fits in the opsin (protein) binding pocket (its basically a term to describe how its bonded together). Thus they split up - This process is called Bleaching.

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16
Q

Visual pigment bleaching happens over a series of steps and isomerisations- but which one is the trigger for transduction?

A

Metarhodopsin II

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17
Q

Is the response in rods faster than the response in cones?

A

NO. The response in cones is faster than the response in rods.

18
Q

What is rhodopsin?

A

Retinal + opsin

19
Q

Remember that a photoreceptor is exactly that- a receptor. It’s state is dependant on what channels are open or closed.

What state are photoreceptors in at rest (i.e. when there is no light stimulating them?

A

They are in what we call Dark current mode. So you just have that natural movement of ions happening in and out of the photoreceptor keeping it in it’s resting state.

(Think back to a level bio and how for pacinian corpuscle you would have the whole leaky channels and the whole 3Na+ out and 2K- going in and out to keep it at its resting potential and volatge)

20
Q

What does the action of light being added to a photoreceptor do?

A

The action of light is to decrease cGMP levels so that the cation channels shut. Thus less cations enter the photoreceptor and it hyperpolarises.

G-protein in the picture is called transducin.

(Should know the steps in the pic)

Steps after the picture:

5) This causes calcium channels to open , causing an increase of calcium.
6) This affects neurotransmitter release at the synapse.
7) Therefore stop the signal going to bipolar cells
8) Which induces a signal in the bipolar cells

[Just note that normally things get depolarised and cause an action potential but not photoreceptors - they get hyperpolarised and cause an action potential]

21
Q

In the CENTRAL retina each cone connects to its own ‘midget’ bipolar cell. This midget bipolar connects to no other cones.

What does each midget bipolar cell connect to?

A

Each midget bipolar cell connects to its own midget ganglion cell.

(This is a one-to-one pathway that carries on till the LGN)

22
Q

What is convergence of information?

A

Coming together of information (think summation).

23
Q

How does rod connectivity with retinal cells occur?

A

This is the same for all over the retina by the way not just the central region.

24
Q

Is there convergence in central cone signals?

A

No

25
Q

Is there convergence in rod signals?

A

Yes

26
Q

Why are cones not very sensitive to light?

A

You need to know the slide.

[The isomerisations need to happen in a short time frame]

The other reason is that each central cone is linked to one bipolar cell and so on. At low light levels there are very few photons available, the probability that sufficient photons are available to all fall on one outer segment at the same time and induce photosiomerisation is low (remember 5 are needed).

27
Q

Why are rods sensitive to light?

A

Because of the convergence.

One ganglion cell will be recieving input from multiple rods, the probability that you get 5 isomerisation events is possible as 5 different rods being activated would activate one ganglion cell (i.e. 5 different rods could recieve one photon each and converge to activate the ganglion cell whereas with central cones - that same cone would have to undergo 5 isomerisations itself to be activated).

Thus there is a higher sensitivity of rods in low light levels.

28
Q

What is visual acuity?

A

It is synonymous with spatial acuity.

Spatial acuity is our ability to resolve detail and is what you will be testing with conventional charts. In its simplest sense, acuity is our ability to resolve 2 points

29
Q

In order to resolve two seperate points how must they be imaged onto photoreceptors?

A

In order to resolve 2 points they must be ‘imaged’ on at least three separate photoreceptors.

If two points were images by two different photoreceptors only then the brain would inteprete them as an oval. However if the two points were ‘imaged’ by three photoreceptors with the photoreceptor in the middle picking up nothing, to determine that they are two dots rather than an oval.

Central cones are perfectly adapted to do this as they have that one to one relation.

[The image is in quotation marks as the photoreceptor in the middle isnt really imaging the spots].

30
Q

What makes rods poor for visual acuity?

A

That summation/convergence of information means seperate points cannot be identified so an oval would be picked up the same way as two spots next to eachother.

31
Q

What is the foveola?

A

The centre of your fovea where it dips.

(You can see from the histological section that in the foveola you have no ganglion cells nor any inner nuclear layer. May be a few muller cells present but they are just holding tissue together - the random three spots you see in the fovea histology section of the dip)

32
Q

How does the foveola have that structure and what is the name given to its development.?

A

So basically the foveola has no ganglion cells nor an inner nuclear layer because it basically pushed them aside during development .

The name given is Lateral Displacement

This whole pit formation also means ganglion axons have to curve around.

33
Q

Where is the highest density of cone photoreceptors?

A

At the Fovea

34
Q

Are there rods in the fovea?

A

No, rods are devoid of the fovea but present in the periphery.

35
Q

How does the size of rods vary?

A

The more peripheral they get, the larger they become.

36
Q

Is the fovea vascular or avascular?

A

The fovea is also avascular (this is actually because of lateral displacement - you have literally moved the inner 5 layers out of the way). It therefore receives all it nutrients from the choriocapillaris, which is more pronounced behind the macula than elsewhere.

37
Q

The fovea accumulates macula pigment (Lutein and Zeaxanthin) what does this mean for it?

A

(When it refers to removing wavelenghts most prone to chromatic aberration and scatter - they are talking about blue light)

(Macular pigment acts as an antioxidant- stopping damage).

38
Q

Why is the foveola highly adapted for high visual acuity?

A

The amount of scattered light is reduced by;

Ø The inner 5 layers of the retina being pushed aside (because having 5 layers would increase the possibility of scatter)

Ø It’s avascular ( so light is not obstructed getting to the photoreceptor + blood is pigmented so scatters light)

Ø The absorption of short wavelengths by the macular pigment (which decreases the amount of Rayleigh scatter and chromatic aberration)

Ø

Also tightly packing in these (thinner) cones that have a one to one relationship with their ganglion cells in a small region of space where we arent getting scatter to increase sampling frequency (i.e. get more megapixels).

39
Q

What is cone type distribution like in the foveola?

A

Directly under foveola we don’t have blue cones.

40
Q

What is cone distribution like in the fovea?

A

Random assortment of red and green cones whereas blue cones are fewer and more structured (s-cones).

41
Q

In a disease that affects the macula are optometrists willing to sacrifice the macula in order to save the fovea?

A

Yes as fovea is from where most of your central vision comes.

42
Q

Why are conditions like AMD particularly debilitating?

What’s an example of the fovea being protected in the case of a disease?

A