S3: Visual Physiology Flashcards
1
Q
Describe structure of cone receptors
A
- The specialised bit of the cell is the outer segment. It consists of stacks of phospholipid bound sacks. The function of these stacks of membrane is for holding in place metabolites (phototransduction is a biochemical reaction that requires enzymes, proteins etc if which many are membrane bound).
- The inner segment contains a nucleus, axon and synaptic terminal that releases glutamate (fast excitatory NT). The ‘axon’ does not fire any AP as it is too small.
2
Q
Describe the mechanism of cone receptors in response to increased light (using RMP)
A
- Remember that photoreceptors are nerve cells that come from the neural tube.
- Therefore, photoreceptors have K+ leak channels and this gives it a negative RMP as K+ leaks out.
- However, the membrane potential is not as negative as in a normal nerve cell and it is more positive at about -45mV. This is because the outer segment has Na+ channels that allow Na + to leak into the cell, adding positive charge making the RMP more depolarised then normal.
- This means the photoreceptor has a intermediate position RMP where it can depolarise or hyperpolarise quite strongly (remember it can’t fire any AP).
- When the amount of light (illlumination) hitting the outer segment increases, some of the Na+ channels close shut which stop much of Na+ going into the cell while K+ continues to leak out.
- This results in the cell hyperpolarising which causes a reduction in the release of glutamate.
3
Q
Describe the mechanism of cone receptors in response to decreased light and how the photoreceptors will respond as an individual looks around the room
A
- When the amount of illumination hitting the retina decreases, there then will be more Na+ open, causing more Na+ flow into the cell causing a depolarisation. This will result in increased release of glutamate.
- As the person looks around the room, the photoreceptor will switch between hyperpolarising and depolarising as illumination decreases and increases. It is equally sensitive to both increase and decrease of light.
4
Q
List steps on transduction (how illumination closes/opens Na+ channels and changes how much glutamate released)
A
- Initiation of light response.
- Amplifying biochemical cascade.
- Termination of the response.
This all occurs in response to one photon but in reality we have lots of photons hitting our retina so this will be happening over again.
5
Q
Explain transduction: initiation of the light response (photoisomerisation of retinal)
A
- Embedded in one of the membrane discs in the outer segment of the photoreceptor, is a protein called opsin.
- The opsin has a binding site for a molecule of retinal (chromoform). The retinal is the area that detects the light and together, the opsin and retinal form the photopigment.
- The retinal when bound to opsin and ready to be activated is called the 11-cis retinal because of its chemical structure. All the carbon bonds are trans bonds except the one at the 11th carbon which is a cis bond and this is a relatively weak bond and a kink in the tail of retinal.
- Hence when a photon of light hits the it, the cis bond breaks and when it reforms, it becomes a trans bond which is more stable creating all-trans retinal.
- This photoisomerisation of retinal is the light sensitive step.
- The sodium channels at this point, are held open by two molecules of cyclic GMP which are intracellular messengers.
6
Q
Explain transduction: amplifying biochemical cascade
A
- At this point, there is activated photopigment which triggers an amplifying biochemical cascade (activating G protein which activates an enzyme) resulting in cGMP to be broken down and its concentration intracellularly to decerease.
- The active opsin, can activate many G protein switch will activate many enzymes.
- The Na+ channels in the outer segment are held open by cGMP so a fall in cGMP will cause some channels to close.
- This is why increased illumination causes decreased Na+ movement into the cell and hyperpolarisation.
7
Q
Describe transduction: termination of the response
A
- There is the need for the response to be terminated as we don’t want transduction to be going on continuously in photoreceptor.
- A process occurs where the trans retinal is taken away to the retinal pigment epithelium (RPE) and glial cells to be converted back to 11-cis retinal.
- The opsin is now inactivated so the biochemical cascade stops and a new enzyme comes in and replenished levels of cGMP so the Na+ channels reopen.
- The 11-cis retinal is then put back into the opsin creating a new photopigment ready to respond.
8
Q
Describe adaptation of our cone photoreceptors
A
- Our cones need to give us strong responses even to minute changes in brightness. So they need to constantly adapt by resetting sensitivity of amplification cascade (by either opening or closing sodium channels to bring membrane potential down to RMP. This occurs due to continuous stimulation that doesn’t change.
- They control the rate and sensitivity
9
Q
What is retinitis pigmentosa?
A
- Defects in many of the necessary proteins result in degenerative disease as the whole transduction process is very complex.
- Retinitis pigmentosa is when there is degeneration from ouside inwards of the retina.
- It is generally driven by a mutation in one of the rod enzymes or proteins and it starts with degeneration of rods and then eventually the entire retinal circuit.
10
Q
What is the result of our photoreceptor outer segments producing a very fast response to light?
A
- We can see a stimulus that is flickering 70 times per second.
- This results in a very high metabolic rate and response so they need a very rapid supply of oxygen and nutrients.
- Photoreceptors use GTP and ATP very rapidly.
- This is usually delivered by a dense capillary bed but this is not possible in the outer layer of the retina as it would block the light path
- A solution is the choriod.
11
Q
What is the result of our photoreceptors being packed tightly together?
A
- Photoreceptor outer segments support high resolution sampling of the visual image by being packed tightly together.
- This is not possible with a normal capillary bed so the choriod is the solution.
12
Q
Describe how our photoreceptors have a highly specialised blood supply
A
- The highly metabolic outer segments of the photoreceptors lay just under the renal pigment epithelium which is a single layer of cuboid cells.
- Surrounding the pigment epithelium on the outside is the choroid blood supply.
- The choroid is a massive blood supply and so efficient and rapid at carrying oxygen to the photoreceptor outer segments so that they are constantly in an environment of arterial partial pressure despite the fact they are constantly using it up and converting it to CO2.
- This is why the outer segments must lay near the choroid because it is the only way of supplying their demand for oxygen explaining why the retina is ‘inside out’ and why outer segments are pointing away from the light.
13
Q
Describe how the retinal pigment epithelium (RPE) sits between the photoreceptors & the choroid
A
- The renal epithelium cells surround the photoreceptors.
- The pigment epithelial cells create sheets that project in between the outer segments (interdigitates),
- The only thing holding the photoreceptors to the RPE is the fact the pigment epithelial cells are sucking fluid out of the gaps in between. This suctioning keeps the retina in place (holding neural retina onto pigment epithelium). This is why if there is a break in the retina that allows fluid to flow into that space faster than the RPE can remove it, then the retina will peel away from the RPE and this is a detached retina.
- Hence one of the functions of the RPE is to hold the retina in place.
14
Q
Describe function of retinal pigment epithelium (RPE)
A
- The RPE cells act as the blood-retinal barrier between outer sements and the choroid. It has tight junctions and control the flow of substances in and out of the retinal tissue. They allowing nutrients in and waste out.
- It will also take the trans-retinal (activated) and convert it to 11-cis retinal which can then be returned back to the photoreceptor.
- It also renews the outer segment membranes of cone photoreceptors. RPE cells act as phagocytic cells and bite the top of the outer segments of photoreceptors, the outer segments then regrow. This is due to photooxidation of lipids and proteins that can occur to the outer segments due to light and this can build up damage molecules.
In this way every 10 days the outer segments are replaced. - It holds the retina in place.
- Also contains pigment granules that absorb stray light.
15
Q
How can RPE be damaged?
A
- Degeneration of RPE is a feature of many retinal diseases.
- Retinoids are molecules that can damage cell membranes, usually they will be chaperoned around to prevent this, but sometimes this can go wrong and cause damage!
- The outer segments and RPE are subject to high oxygen concentration as well as electromagnetic radiation (light!), these combined can cause photo-oxidation. Unfortunately it is phospholipids and proteins (the very substances that the outer segments are made of) that are easily oxidised. This is partly why the outer segments must be replaced regularly, in order to remove damage regions.
16
Q
How can ‘drusen’ occur?
A
- If damaged parts of the outer segments on photoreceptors are not removed, the damaged molecules tend to hang around.
- With age, the RPE tends to become clogged with intracellular debris (called lipofusin). Some of this comes from photo-oxidised proteins and phospholipids of retinal image.
- It seems the RPE gets rid of some of this debris by depositing it onto the basement membrane, where it attracts cholesterol and immune cells from the blood which builds up fatty plaques (called drusen). This is because damaged lipids and proteins can’t be digested by RPE.
- Where there is drusen, there is likely to be death of photoreceptors as they are blocking movement of oxygen and nutrients from the blood. This is partly why vision decreases as we age, as the photoreceptors are being killed off in this way.
17
Q
What are the ganglion cells in the retina?
A
- The ganglion cells are the afferents of the system. They are linked to the photoreceptors by bipolar cells.
- Each cone photoreceptors (of which there is only one array) will provide input to one of several populations of ganglion cell.
18
Q
List the 4 types of ganglion cells
A
- ‘Off’ cells.
- ‘On’ cells.
- ‘Parvocellular’ cells.
- ‘Magnocellular’ cells.
19
Q
Describe ‘off’ and ‘on’ ganglion cells
A
- ‘Off’ cells are excited by decreased illumination of their photoreceptors over their receptive fields.
- ‘On’ cells are excited by increased illumination of their photoreceptors.
- This is interesting because despite the photoreceptor itself hyper-polarising and having reduced firing on increased illumination, some ganglion cells will be excited.
- So although all photoreceptors will be depolarised by decreased illumination, this is only true for half of the ganglion cells, the other half are excited when light falling on their receptive field increases.
20
Q
What is the fuction of parvocellular ganglion cells?
A
- These are specialise for high resolution and colour (have small receptive fields so input is from one or two cones),
- They extract fine detail and colour information.
- They only work well when image is stable as they are insensitive (if image is moving these GC don’t work well).
21
Q
What is the function of magnocellular ganglion cells?
A
- These are specialised to detect fast moving objects and low contrast objects (broad outlines).
- They receive input from many cones and rods.
22
Q
Describe mechanism of parvocellular ganglion cells for fine detail using the parvocellular receptive field
A
- The parvocellular ganglion cells which are involved in the pathway for fine detail have very small receptive fields with one or two cones.
- If just this central receptive field experiences a change in illumination, then the ganglion cell will respond.
- However, the get fine responses, as well as a small receptive field, there needs to be lateral inhibition of surrounding areas.
- If the yellow ganglion cell has change in illumination just in its central receptive field, then the inhibitory interneurons will be activated by the corresponding cone and inhibit the surrounding cones. This enhances and pin points the visual information seen by that ganglion cell and allows fine detail.
- Alternatively if there is illumination of a wider area, covering the receptive field and surrounding area then the retinal ganglion cell will get inhibited by the interneurons due to activation of surrounding cones.
23
Q
Describe how retinal ganglion cells respond to contrast between the illumination of centre and surround
A
- A parvocellular ganglion cell will only fire when there is excitation in the centre of its receptive field and not fire if it and its surroundings are excited to an equal extent because the inhibition and excitation will cancel out.
- Thus parvo ganglion cells only respond to contrast and thus allow us to see edges. This is because where a ganglion receptive field is on the edge, it is receiving different information to the surrounding and therefore will be excited (the brain will recognise this specific response and allow us to see edges).
- The ganglion cells receptive fields that cross the edge will be receiving different levels of brightness and info coming in from the visual world. Hence the photoreceptors will be activated differently and the inhibition will not cancel out everything, rather the ganglion cell will be activated and the brain recognises this information as meaning an edge.
24
Q
How does our brains get confused when retinal ganglion cells respond to contrast between the illumination of centre and surround? (with example)
A
We witness this in optical illusions.
This is because our brain is enhancing the edges, telling us that the bar is brighter against the dark background and darker against the white background.
The brain isn’t getting information about the centre of the bar, so it interprets it as being shaded.
25
Q
Describe mechanism of magnocellular ganglion cells increased sensitivity at the expense of resolution using the magnocellular receptive field
A
- At any given location in the retina there will be both parvo and magno cells, but the magno cells have a much larger receptive field.
- These large receptive fields are created by convergence of inputs from many photoreceptors, this makes the magno cells more sensitive to faint objects or fast moving objects.
- This is because something that a parvo cell may miss because the fast moving object moved to fast, will be picked up by the magno cell because it is linked to many photoreceptors which would have picked it up.
- It does this at the expense of resolution.
26
Q
How do we see colour with ganglion cells?
A
- Light is a form of electromagnetic radiation and we can only see a small portion of its wavelengths, which our brain interprets as colour.
- To do this we have three types of cone photoreceptor which respond most effectively to long, medium and short wavelength light, “red”, green” and “blue” respectively.
- Our cones responses to wavelength do overlap, hence the response of a single cone is ambiguous. Because of this, in order to identify colour the brain must compare the responses of cones.
- Red is compared with green and blue is compared with yellow (combined red and green). This is because if we take a blue wavelength, it will produce different absorption for the red cones and green cones and same for red and green.
27
Q
Why is colourblindness for common in men?
A
- The genes for the red and green photoreceptors are on the X-chromosome, this makes colour blindness much more common in men! Specifically red-green defects.
- Colour blindness is rare in women because they have two X-chromosomes and require two mutated copies.
28
Q
What does the primary visual cortex encode?
A
Retina and lateral geniculate nucleus cells encode: - Contrast (edges of things). - Wavelength. Other cells: - The orientation of edges. - The presence of corners etc. - Direction of motion, - Binocular disparity (slight difference in image from two eyes and the inputs merge in primary visual cortex).
29
Q
How can our eyes be fooled to see depth?
A
By sending in different input from two eyes. This is how 3D films work.
30
Q
Describe how the higher visual pathway processes shape and form
A
All visual information from the retina goes to the primary visual cortex. From here the information is sent out to various cortical areas.
- Higher visual cortex are areas that run along the base of the temporal cortex. These are the inferotemporal pathways.
- This pathway is involved in telling us information about prior experience and recognising what something is, what it means and its shape and colour.
- Here, information from the eyes is combined with information being fed down from the frontal cortex.
31
Q
Describe
Associative agnosia
A
This is ‘normal percept stripped of meaning’. This is where a normal percept is stripped of meaning. Damage to these inferior temporal pathways which enable us to know what we’re looking at will mean an individual can indeed see something and copy it.But if asked what it is they will be unable to say as they have lost this ability.
32
Q
Describe how the higher visual cortex processes location and movement
A
- Another higher visual cortex pathway is one that runs into the parietal cortex. It actually slides up against the sensory strip.
- This pathway receives great input from the magnocellular ganglion cells in the retina.
- These parietal regions are involved in movement and spatial vision (Telling us where an object is and where it is going, how an object relates to other objects (e.g. a doorway) and whether we are moving or the object is moving).
33
Q
Describe how the higher visual cortex is involved in control of self-movement
A
The parietal areas interact with motor and somatosensory cortex! This pathway tells us how can we interact with the object.
34
Q
What is conjugate eye movement and disconjugate eye movement?
A
Conjugate eye movements is both eyes moving at same speed and in same direction while disconjugate eye movements is both eyes moving at in different directions.
35
Q
Describe the pathway for reflex saccade (type of conjugate eye movement)
A
- The pathway for a reflexive saccade goes straight from the retina to the brainstem, precisely the superior colliculus (central controller for saccadic eye movements). So the retina is informing the superior colliculus that something unexpected has happened.
- The superior colliculi control various nuclei in the brainstem, these particular nuclei are called gaze centres because they control where we are looking at.
- Vertical gaze centres contain nuclei that have control of the motor nerves that control vertical movement of the eye.
The vertical gaze centre when excited will send impulses to the trochlear nucleus or oculomotor nucleus and this will cause the elevation or depression of the eye. - The horizontal gaze centres contain nuclei that control the motor nerves that innervate muscles that cause horizontal movement. The horizontal gaze centres when excited will send impulses to the abducens nucleus (for example) and this will cause abducens nerve to fire and cause abduction of the eye. In another situation it may activate the CN III nuclei to adduct the eye.
36
Q
Describe the pathway for exploratory saccade (type of conjugate eye movement)
A
- When we see an image e.g. a giraffe, the eye will scan over it to find the important features so that the brain can recognise what it is. This is a reflexive movement, that is happening under cortical control because the visual cortex is deciding where to look.
- This is a reflexive action and enacted by the superior colliculus, however in this saccade the colliculi are being driven by the area of visual cortex involved in spatial vision, this is in the parietal cortex.
37
Q
Describe the pathway for voluntary saccade (type of conjugate eye movement)
A
- When your eye glance at something you want to look at e.g. clock, this is a voluntary saccade.
- The voluntary saccade is being driven by the frontal cortex (a specific area called frontal eye fields) which acts via the superior colliculi (because it controls eye movement) which is in control of the gaze centres and these control the extraocular eye muscles.
38
Q
What are the three saccades for conjugate eye movement?
A
- Reflex saccade.
- Exploratory saccade.
- Voluntary saccade.
These are the three saccades and indeed most of the eye movements we make are jumps.
39
Q
Describe the pathway for smooth pursuit (type of conjugate eye movement)
A
- There is one type of eye movement which is not a saccade rather you make smooth eye movements.
This is when we are tracking the movement of something with our fovea, e.g. a wasp buzzing around and these type of eye movements are called pursuit. This needs to be accurate so we can keep image in our fovea - eye movements may compensate for body movement. - Smooth movements are coordinated by the pontine nuclei. They can be driven the frontal eye fields which is the voluntary part and the superior temporal areas which are movement sensitive which log whether the object we are trying to keep in our fovea has moved out and get our eyes to keep up with it.
- These inputs ensure the pontine nuclei are given information on the accuracy of movement and if any innacuracies have occurred (superior temporal input) and the frontal input is what gives the voluntary aspect. The decision to follow it in the first place.
- The pontine nuclei send information to the cerebellum which then feeds it down to the vestibular nuclei.
40
Q
Why can we retain saccadic movements but lose smooth movement in our eye (or vice versa)?
A
Pursuit movements are driven by a completely different set of pathways to saccades, thus it may happen that an individual loses ability to make pursuit movements but retains saccades or vice versa.
41
Q
What is the role of the vestibular nuclei for smooth movements of the eye?
A
- The vestibular system is the organ of balance! One of the very important things it does is to track head movements. This is because if we are trying to track something with our eyes and keep moving our head our visual field will get wonky unless our eyes turn to compensate.
- Thus, it is actually the vestibular nuclei that has the final control of the extraocular motor neurones. The vestibular nuclei bring together the visual and vestibular information to produce coordinated and accurate eye movements.
42
Q
Describe the pathway for convergence (type of disconjugate eye movement)
A
- Disconjugate eye movements are when the eyes are moving in different directions to one another. The main reason we do this is to look closer (both eyes are moving in the opposite direction, to come together and compare items far and close).
- This goes through a different pathway to conjugate movements.
- Convergence starts with the visual cortex giving the desire to look at something close (as voluntary). The visual cortex has axons go to the vergence centre which then activates the oculomotor nucleus. This causes the oculomotor nerve to fire which causes the medial rectus muscle to contract turning the eyes inwards.
- At the same time, the vergence centre activates the Edinger-Westphal nuclei, these nuclei send parasympathetic axons to the ciliary ganglion. Their activation will cause two things to occur via the short ciliary nerves (post ganglionic nerve). It will contract ciliary muscle, causing zonular fibres to relax and lens will fatten up allowing close vision. It will also constrict the pupil which improves focus.
