Visual system- retina to cortex Flashcards
What are horizontal and amacrine cells thought to be involved in
Setting up centre-surround visual fields, enabling lateral inhibition to provide greater contrast
What allows high acuity in the fovea for cones
Often a 1:1 relatinoship between cones/bipolar cells/ganglion cells meaning low convergence, small receptive fields, densely packed
What is sacrificed for high acuity in cones at the fovea
Sensitivity
What reduces acuity but improves sensitivity at the peripheral retina for cones
More convergence of cone info -> bipolar cell info -> ganglion cell info
Why does it make sense for our cone periphery to be high sensitivity but low acuity
It is more important our periphery is sensitiive so we can notice things, then turn and use our foveally dominated vision for detail
How sensitive vs high acuity are the rods
Low acuity, very high sensitivity
Why is rod vision low acuity but high sensitivity
Info from many rods converges onto a single rod bipolar, which is compressed again by ganglion cells
Why does convergence reduce acuity
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
Sensitivity and accuracy of scotopic vs photopic vision
Scotopic vision- very sensitive, not very accurate
Photopic vision- very accurate, not very sensitive
How do amacrine cells affect rod vision during mesopic conditions
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)
What are amacrine cells sometimes called for their role in mesopic vision
Piggyback cells
What is the result of the ganglion cells receiving a mix of info from rods and cones in mesopic conditions
Vision has a balance between acuity and sensitivity
What is the pathway taken by info in mesopic conditions in the retina
Rods ->Rod bipolars -> All amacrine cells -> Cone bipolars -> Ganglion cell
What conformational change marks the start of phototransduction
Photons induce a confirmational change in retinal (cis retinal -> trans retinal), which activates the opsin (a GPCR) that activates the G protein transducin
What is the opsin in rods
Rhodopsin
What are the opsins in cones
Photopsins- 3 types; red, green, blue
What is the effect of the activation of G protein transducin in phototransduction
Transducin triggers phosphodiesterase (PDE) to hydrolyse cGMP, reducing cGMP levels which closes cGMP-gated channels
What is the effect of cGMP-gated channels closing in phototransduction
The photoreceptor hyperpolarises in a graded manner, as Na+ can no longer enter through the channel
What is the result of graded hyperpolarisation of photoreceptors due to phototransduction
Corresponding graded reduction in the rate of neurotransmitter release onto bipolar cells
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
Light hyperpolarises the cone, at the highest light levels the response is saturated and the receptor is said to be bleached
What is the sensitivity to bleaching of rods vs cones
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
What 4 mechanisms terminate the phototransduction cascade
Inactivation of rhodopsin, inactivation of transducin, inactivation of phosphodiesterase (PDE), activation of guanylate cyclase
Phototransduction cascade termination- what causes inactivation of rhodopsin
Rhodopsin is phosphorylated by the opsin kinase, then arrestin binds to phosphorylated rhodopsin, completely deactivating it- resuming dark current
What happens to rhodopsin in the dark
Rhodopsin regenerates after being bleached
What underlying intracellular factor drives termination of the phototransduction cascade
Low intracellular Ca2+ levels caused by closing of cGMP-gated channels by high light levels
What is the purpose of termination of the phototransduction cascade
Allows light adaption of the bleached photoreceptor, so membrane can be gradually depolarised to about -35mV again and we can see again
Phototransduction cascade termination- what causes inactivation of transducin
Occurs through the hydrolysis of bound GTP to GDP, via an intrinsic GTPase activity
Phototransduction cascade termination- what causes inactivation of phosphodiesterase (PDE)
The inactivation of transducin causes it to dissociate from PDE, resulting in a cessation of PDE-mediated cGMP hydrolysis
Phototransduction cascade termination- what causes activation of guanlyate cyclase
Guanylate cyclase is activated by gualynate cyclase activating protein (GCAP), restoring cGMP levels and promoting the reopening of cGMP-gated channels
What 2 types of bipolar cell receptive field are there
ON-centre, OFF-centre
What maximally excites an ON centre bipolar cell
Light in the centre of the receptive field, dark in the surround
What maximally excites an OFF centre bipolar cell
Dark in the centre of the receptive field, light in the surround
What do bipolar cells respond to rather than light an why
Local contract, as they receive opposing input from surruonding receptors
Why does it make sense for bipolar cells to respond to contrast rather than light
We are interested in seeing edges andnot uniform illumination or darkness
Who is credited with discovering centre-surround receptors
Kuffler (1953)
How do the centre-surround receptive fields of bipolar cells allow lateral inhibition
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
What is the physiology behind the lateral inhibition of eg ON-centre bipolar cells
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
What would be the result of uniform light on the ON-centre or OFF-centre bipolar cell receptive field
No net response, as activation of the centre/surround will cancel out the surround/centre
Study showing the effectof light presented in different parts of the bipolar cell receptive fields
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
What dictates whether a bipolar cell is ON or OFF centre
OFF and ON bipolar cells express different glutamate receptors on their dendrites
What glutamate receptors are expressed in OFF vs ON bipolar cells
OFF- AMPA
ON- mGluR6
Response of OFF bipolar cell to glutamate
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
Response of ON bipolar cell to glutamate
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
Study showing effect of inactivatnig ON-centre bipolar cells in monkeys- procedure
Schiller et al (1986)- pharmacologically inactivated ON centre bipolar cells in monkeys, using blocker amino phosphonobutyrate (ABP)
Study showing effect of inactivatnig ON-centre bipolar cells in monkeys- results
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
What are ON bipolars also called
Invaginating cone bipolars
What are OFF bipolars also called
Flat cone bipolars
How do the connectinos between bipolar cells and ganglion cells differ
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
When is the max response of ON centre retinal ganglion cells
Max response when light in the centre, and dark in the surround
When is the max response of OFF centre retinal ganglion cells
Max response when darkness in the centre and light in the surruond
How do both ON and OFF retinal ganglion cells response to luminance contrast (either from light in centre/dark surround or vv)
Increased firing patterns
What is an OFF centre RGC doing when an ONcentre RGC is firing at its highest level
OFF centre RGC is completely silent
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
OFF-centre RGC- dark in the centre causes depolarisation, dark in the surround causes hyperpolarisation
Response of OFF RGCs to a light/dark edge- no stimulation of receptor field
Weak basal level of signsl
Response of OFF RGCs to a light/dark edge- edge of dark light enters surround only (only edge of surround is dark)
Hyperpolarisation, reduction in signal
Response of OFF RGCs to a light/dark edge- edge of dark light starts to include the centre
Partial inhibition by darkness in surrouns is overcome, APs increased due to depolarisation of centre
Response of OFF RGCs to a light/dark edge- dark light fills whole surround
Depolarising dark centre response is cancelled out by the hyperpolarising surround response
How is info about increases and decreases in luminance carried to the brain
By axons of 2 seperate bipolar and RGC types in parallel pathways
What do RGC cells respond to just like bipolar cells
Edges/contrast- light regions stimulation ON ganglion cells and dark regions simulate OFF ganglion cells
What are the 5 main types of RGC
P type, M type, non M non P, photosensitive ganglion cells, ganglion cells projecting to superior colliculus
Which one of the 5 main RGC types are not invovled in perceptual vision
Photosensitive ganglion cells
What is the proportion of the different types of RGC
90% parvocellular
5% magnocellular
5% koniocellular
What are P type RGCs
Parvocellular cells, historically called midget cells due to small dendritic tree
What are M type RGCs
Magnocellular cells, historically called parasol cell due to extensive dendritic tree
What are non M non P type cells
Koniocellular cells, less well characterised, many subtypes
What do photosensitive ganglion cells contain
Photopigment melanopsin
Where do photosensitive ganglion cells project
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
What do ganglion cells projecting to the superior colliculus have a role in
Saccadic eye movement
Receptive field size for P cells vs M cells
P cells- much smaller receptive fields, can discern detail
M cells- larger receptive fields
Speed of conduction for P cells vs M cells
P cell axons conduct impulses much more slowly than M cells
Sustained vs transience of response of P cells vs M cells
P cell responses, especially to colour, can be sustained
Responses of M cells are much more transient
Response to colour and contrast of P cells vs M cells
P cells- sensitive to colour, require high contrast stimuli
M cells- not sensitive to colour, more sensitive to low-contrast, black and white stimuli
What are the distinct functional properties of M and P type cells the start of
Parallel processing in the visual system
Function of M type cells
Highly sensitive to low-contrast stimuli and rapid movement visual signals
Function of P type cells
Detection of visual signals relating to fine details and high contrast, relatively insensitive to low contrast stimuli and rapid movement visual signals
Do the M cells mean humans have motion sensitive RGCs?
No- the M cells feed into the motion pathway at HIGHER levels of the visual pathway (Bach, 2000)
What can the receptive fields of P type ganglion cells show due to their sensitivity to colour
Red/green colour opponency
What are the 4 types of centre-surround receptive fields of P type cells
Green-centre ON/red centre OFF
Green centre OFF/red centre ON
(and vv w red centre)
What can the receptive fields of non M/non P type ganglion cells show
Blue/yellow colour opponancy
What creates yellow in blue/yellow opponancy in non M/non P ganglion cells
Combination of red and green cones
Who discovered the morphology of the blue ON/yellow OFF ganglion cell
Dacey and Lee (1994) via intracellular recordings and staining of these ganglion cells in monkey retina
What types of blue/yellow opponency cells are there
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
What does SCN stand for
Suprachiasmatic nucleus
How are individual cones entirely colour blind
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
What is the consequence of individual cones being entirely colour blind
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
How is the ambiguity of discriminating colours based on photoreceptor activity resolved
Opponent mechamisms- comparing the activity in different classes of cones at the same point in time to extract colour info from stimuli
What are the 3 opponent mechanisms used in discriminating colours
Comparing difference between R and G cones, B and (R+G->Y) cones, achromatic mechanisms for detecting differences in luminance/contrast
How would a red ON centre/green OFF surround P ganglion cell respond to- red light on centre
Red cones in centre are activated, leading to RGC depolarisation and increased activity
How would a red ON centre/green OFF surround P ganglion cell respond to- overall red light
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
How would a red ON centre/green OFF surround P ganglion cell respond to- red light in centre, green light in surround
No response- depolarising response to red light in centre is cancelled by the hyperpolarising response to green light in the surround
What is the most common form of colour blindness and how is it linked
Red-green colour blindness is sex-linked
Why were colour blind people useful in WW2
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
What can red/green opponent P ganglion cells respond to other than colour
Responses of red and green cones are used to detect luminance changes, providing fine detail of P pathway while being achromatic
How can red/green opponent P ganglion cells respond to luminance changes
White light contains all the spectrum of colours, so will include some red and green wavelength light
What are M type ganglion cells called in terms of their receptive fields
Broad band cells
Why are M type ganglion cells called broad band cells
Large receptive fields, get combined input from red and green cones in both the centre and surround
What are the 2 types of M type ganglion cells
Red and green ON centre/ red and green OFF surround
Red and green OFF centre/red and green ON surround
What do M type ganglion cells measure and why
Can only measure brightness contrast as they are colourblind because they have both R and G cones in both centre and surround
What is the structure of amacrine cells
Lack axons, large dendritic trees, different types connect to different bipolar cells and/or ganglion cells
Are most amacrine cells inhibitory or excitatory
Most are inhibitory using GABA, glycine or dopamine
How do amacrine cells respond to illumination compared to bipolar cells
Amacrine cells respond transiently to illumination giving ON-OFF responses, compared to the sustained response of bipolar cells
Who showed how ganglion cell responses are built from the interactions of horizontal and bipolar cells
Dowling and Werblin (1970s)
Where are synapses between photoreceptors and bipolar/horizontal cells located
In the outer plexiform layer
How many photoreceptors do bipolar cells receive input from in the central fovea vs peripheral retina
Bipolar cells receive input from a cluster of photoreceptors ranging from 1 (in central fovea) to thousands (in peripheral retina)
How do the horizontal and amacrine cells differ in their location of function
The lateral connections of amacrine cells integrate bipolar input to ganglion receptive fields, while horizontal cells provide photoreceptor input to bipolar cells
What phenomenon supports the existence of photosensitive retinal ganglion cells
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
How do photosensitive retinal ganglion cells differ to photoreceptors
Photosensitive retinal ganglion cells depolarise to light, have very large receptive dendritic fields, and there is only a few thousand
What are the only source of retinal output through the optic nerve
The ganglion cells
How are ganglion cells different to all other retinal cells in their electrical transmission
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
What form of organisation does the retina have
Laminar organisation, cells are organised in layers
What is contained in the outer segment of photoreceptors
A stack of membranous disks with light sensitive photopigments in their membranes that absorb light
How does the structure of rods and cones differ
Rods- long cylindrical outer segment containing many disks
Cones- shorter, tapering outer segment with fewer membranous disks
Why are rods over 1000x more sensitive to light than cones
Due to the higher no of disks and higher photopigment conc in rods, plus rods amplify the response to light more than cones
What is a consequence for colour perception of the lower no of cones in our peripheral retina
We are poorer at discriminating colours on our peripheral retina
How do we see colour at night
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
What is the dark current
The steady influx of Na+ through cGMP gated channels in the photoreceptors that keeps the membrane potential at about -30mV IN THE DARK
What is rhodopsin’s structure
Consists of receptor protein opsin, and prebound agonist retinal
Why is the confirmatinoal change in retinal, activating opsin, called bleaching
It changes the wavelengths absorbed by the rhodopsin as the photopigment turns from purple to yellow
How does the biochemical cascade in phototransduction make our visual system very sensitive to light
Signal amplification- each photopigment molecule activates many G proteins, and each PDE enzymes breaks down many cGMPS molecules
What causes the rods to not work in bright light
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
How does phototrasnductin differ in cones and rods
Cones have different opsins in their membraneous disks
What are the 3 different opsins cones can contain
Short wavelength ‘blue’ cones, medium mavelength ‘green’ cones, long wavelength ‘red’ cones
Preferred wavelength of blue cones
430nm
Preferred wavelength of green cones
530nm
Preferred wavelength of red cones
560nm
What determines colour perception
The relative contributions of short medium and long wavelength cones to the retinal signal
Who proposed the 3 cone type idea first
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
What is the dominant theory of colour vision cauued
Young-Helmholtz trichromacy theory
What causes colourblindness
One or more cone photopigment types is missing
What is achromatopsia
Lack of colour vision
Study showing example of achromatopsia
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
What happens in dark adaption
Over minutes-hour, all-cone daytime vision transitions to all-rod nighttime vision, with light sensitivity increasing a millionfold in this period
What does the pupil do to allow dark adaption
Pupils dilate allowing more light to enter the eye, but this only increases light sensitivity by a factor of about 10
What is the main cause of dark adaption
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
What happens when a dark adapted eye goes back into bright light
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
What happens to membrane potential in the process of light adaption
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
What is Ca2+ doing when the cones are in the dark
Ca2+ enters the cones through cGMP-gated Na+ channels, and inhibits guanylyl cyclase that synthesises cGMP
How does Ca2+ allow light adaption when we step into bright light
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
How is the membrane able to be gradually depolarised again in light adaption
Ca2+ allows cGMP channels to open again via a cascade, despite light level not changing
What is the purpose of light and dark adaption
Ensures photoreceptors are always able to register relative changes in light level, though info about the absolute level is lost
