Vision Flashcards
What is the range of wavelengths of visible light
What does this correspond to
~390 (violet) to 700 (far red) nm
The spectrum of sunlight
What are the 4 basic variables analysed by the visual system
Intensity (1) and Wavelength(2) and their variation in space (3) and time (4)
What is light from a light source quantified as
As illuminance (lux)
How is light reflected from objects quantified
Luminance (cd/m^2)
From visual threshold to saturation, by how much can light intensity in the environment vary
What about for reflectance of natural objects
By a factor of ~10^10
Reflectance it natural objects varies nobly ~20 fold and is independent of illuminance
What is the most commonly used measure of light stimulus strength
Relative intensity or contrast
ΔI / I
Where I= mean background
And ΔI= increment in intensity
Briefly give an overview of how an image is formed in the eye
An inverted image is focussed by the cornea and lens on to the retina, with an aperture controlled by the pupil
How are size and distance in the outside world expressed in the retina
In angular terms
As size and distance are expressed in angular terms on the retina, what is 1 degree equivalent to
1 degree = 60 arc minutes
This is about the width of a thumbnail at arm’s length or 300μm on the retina
What is 1 radian in degrees
~57 degrees
What is diffraction
The spreading of waves around objects
Such as light spreading out as it passes through an aperture
What is the point spread function
Express this as an equation
Because of diffraction, even with perfect lenses, the image of a point source is a blurred circle
The angular diameter of point spread function is:
d~ λ/D
Where D= diameter of lens (or aperture if limited by diaphragm or pupil);
λ= wavelength
d~λ/D
What does this mean for the diffraction limit in relation to the lens size
The smaller the lens/ aperture, the larger the diffraction limit
True or false
Lens aberrations degrade the image
True
Other than diffraction, the image can, in practise, be further degraded by optical imprecisions including spherical and chromatic aberration and glare
What is spherical aberration
For a spherical surface, rays towards the edge are more strongly refracted
What is chromatic aberration
Different colours are focussed at different depths
The human eye is well focussed for green but poorly for blue light
Describe how glare can affect image formation
Small particles in the optical media scatter light in all directions, reducing contrast of the image
When does the point spread function approach the diffraction limit
At small pupil diameters when spherical and chromatic aberration is modest
What happens to the point spread function when the pupil dilates
Off axis rays contribute to image formation and aberrations become more significant, broadening the point spread function despite the reduced effects of diffraction
Do eyes have refractive defects
Some eyes may have refractive defects such as ametropic
What does emmetropic mean
Can focus sharply on an object at infinity
If an eye cannot do this it is ametropic
What is myopia and what is its incidence
Short sight
20% of population
What is hypermetropia
How common is it
Long sight
30% of population
What does myopia predispose
Retinal detachment, degeneration and glaucoma
What leads to bifocal lenses being required
Combination of myopia and presbyopia
True or false
Myopia is inherited
False
It has both genetic and environmental factors
What sets an absolute limit on our spatial resolution
Optical quality
WHat does the detail in an optical image have to be matched by
The grain (receptor spacing) of the retina
Theoretically what should the receptor spacing be in order not to sacrifice the detail in the image
Where is this achieved
~half the width of the point spread function
In the fovea
How are adjacent cones arranged in the fovea
Separated by 0.5 arc minutes
Arranged in a precise mosaic to maximise packing density
What are the 4 optical surfaces in the eye
How are they arranged
Front and back surfaces of the cornea and lens
In series
Describe the structure of the cornea
Consists of a 650μm thick layer of transparent collagen fibrils (stroma) encloses between an epithelium and an endothelium
What are stroma in the cornea
Transparent collagen fibrils enclosed between epithelium and endothelium
How is the eye lens structured
Built from long ribbon like cells, packed with transparent protein (crystallin)
Is the lens exactly the same as an adult and child
No
Cells are added to the periphery of the lens throughout life
The lens absorbs increasingly strongly in the blue with age
Where are the oldest cells of the lens
Oldest cells in the core
Where is the greatest refractive index of the eye lens
Why
At the centre
This is to correct for spherical aberration
True or false
The lens absorbs weakly in the UV
False
Absorbs strongly in the blue
What are cataracts
When is this common
Clouding of the lens
In old age
How are the lens and cornea supplied with blood
They are avascular so are supplied with metabolites by the aqueous humour
What is the aqueous humour of the lens and cornea secreted by
How is it drained
What is the primary cause of a glaucoma
The epithelium of the ciliary body
Through the trabecular meshwork and Canal of Schlemm.
A reduction in the rate of flow of the aqueous humour
How is the Power (P) of a lens expressed
Dioptres
1
——————-
Focal length in meters
To a first approximation, how is the power of a lens system in series calculated
By the sum of the powers of the individual components
What is accommodation
The lens changing its focal length to focus on objects at different distances
How is accommodation accomplished
By a combination of radial elastic ligaments (suspenseful ligaments or zonule) and a circular ciliary muscle
What happens when the ciliary muscle is relaxed
The suspension ligaments stretch the lens, reducing optical power
What is focused on the retina when a normal eye is at rest
When contracted?
An object at infinity ♾
Nearer objects
How does lens elasticity change with age
What does this lead to
Decreases with age
Presbyopia- a reduction in accommodating power
True or false
The ciliary muscle is under PS control
True
Via the oculomotor nerve
What is the near reflex
Accommodation combined with simultaneous constriction of the pupil to improve depth of focus and also convergence of the 2 eyes to fixate on the new target
How many muscles comprise the iris
2 antagonistic smooth muscles under ANS control
Sphincter (parasympathetic)
Dilator (sympathetic)
What is pupil diameter largely determined by
What is the control circuit
The sphincter muscle
Involves projection from the retina to the pretectum in the midbrain, which projects bilaterally to preganglionic PS neurons in the Edinger- Westphal nucleus that project via the oculomotor nerve to the ciliary ganglion, innervating the pupillary sphincter muscle
True or false
Illumination of one eye evokes pupil constriction in both eyes
What kind of response is elicited
True - there is a bilaterally projection from the pretectum in the midbrain
It is a direct and consensual response
Where is the pretectum
In the midbrain
What does the direct, consensual response of both eyes constricting for illumination of one eye provide the basis for
A standard neurological test for intact brainstem function in unconscious patients
What is Argyll-Robertson pupil characteristic of
What happens
Neurosyphilis
Pupil does not react to light but does react to accommodation
Which layer are the photoreceptors in the retina
The layer furthest from the incident light
The remaining layers contain visual interneurons
What can glare in the visual interneuron layers do
What acts to reduce the effect of this
Degrade the image
Retinal glial cells (Müller cells) which act as optical waveguides to aid transmission of light
Where are the visual interneurons in the primate fovea
What is the size of the primate fovea
Displaced to the side
1.5mm (5 degrees in diameter)
True or false
Come density increases in the fovea
True but at the expense of rods
What is the foveola?
Is it avascular
How many rods are here
The central 1 degree (260 μm) of the fovea with the highest acuity
Yes - to avoid/ minimise light scattering
The foveola is completely rod free
When is the minimum come spacing reached in the fovea
At the centre of the foveola
How does the fovea and surrounding region reduce effects of chromatic aberration
Contain blue absorbing macular pigment
When does primate rod density peak in the retina
What is the area called
20 degrees either side of fovea
Parafoveal region - this is the area of most sensitive vision under mesopic and scotopic
How are the cones and rods spaced in the parafoveal region
Rods are spaced as closely here as cones in the retina
But rod signals are summed or pooled together, reducing spatial acuity
Where is the eye’s blind spot
Subtending 5 degrees at the optic disk where the optical nerve exist the retina
Why can papilloedema occur
What can happen
Because CSF in the optic nerve is in continuity with that of the brain
The optic disk can appear swollen with raised intracranial pressure
What do both rods and cones consist of
An outer segment specialised for transduction joined to an inner segment with more normal cellular machinery
They are connected by a cilium
What do rod outer segments consists of
Stacked membranous discs containing the visual pigment and enzymes of the transduction cascade
What do cone outer segments consist of
Continuous folds of invaginating lamellae
What is the visual pigment
Rhodopsin
A protein with 7 transmembrane helices embedded in the disk membrane (a prototypical GPCR)
What does rhodopsin bind
A chromophore molecule, 11-cis retinal
True or false
Free retinal only absorbs ultraviolet
True
This changes when retinal is bound:
Interactions between covalently bound retinal and opsin shift the wavelength of peak absorption to ~500nm
Do cone opsins bind an identical chromophore to rods?
Chromophore is identical but different charge interactions tune the absorption to different wavelengths
What happens following absorption of a single photon
What does this lead to
The chromophore isomerise from 11-Cis to all-trans retinal
This photoisomerisation leads to a catalytically active form of rhodopsin known as metarhodopsin II
What is R*
Catalytically active metarhodopsin
What happens once R* has completed its role
all-trans retinal dissociates slowly from opsin
Rhodopsin is now in its bleached form and must be regenerated before it can be used again
How long does it take for all trans retinal to dissociate
100-1000s
Can regeneration of bleached rhodopsin occur within the photoreceptor itself
No
It must be performed in the retinal pigment epithelium (RPE)
What is the RPE
Retinal pigment epithelium
The cells of which encompass the apical processes of the outer segments
Describe the process of photo pigment regeneration
Retinal is reduced to all-trans-retinol, which is transported out of the photoreceptor to the RPE
It is then converted back to 11-cis-retinal
It is then transported back to the photoreceptors where it rejoins the bleached opsin to form rhodopsin
After bright light how long can it take before rhodopsin is fully regenerated
30 minutes or more
What is retinal derived from
Vit A
What can vitamin A deficiency lead to
Night blindness
What is vitamin A
11-cis-retinol
Where can rapid rhodopsin regeneration occur
There is an alternative pathway via Müller cells which allows rapid regeneration in cones
How does phototransduction take place
Overview and specifically (give cascade)
Via a GCPR cascade, culminating in the destruction of cGMP (a negative internal transmitter)
R* activates transducin (a G protein)
Transducin and rhodopsin diffuse freely in the disc membrane
Each transducin molecule activates 1 PDE
PDE hydrolyses cGMP into inactive 5’GMP
Reduced cGMP results in closure of cyclic nucleotide gated cation channels, leading to a hyperpolarising response
How many transducin molecules can R* activate
by random collisions R* can activate >1000 transducin molecules
What is a PDE
Phosphodiesterase
Which molecule is in high concentrations in rod cytosol in the dark
Why is this
cGMP
cGMP continuously opens cyclic nucleotide gated cation channels, preventing a hyperpolarising response
How is a response to light terminated in rods
Guanylyl cyclase resynthesises cGMP
Is rhodopsin the only intracellular signal transduction cascade involving G proteins?
Eg?
No
Other cascades use GPCRs homologous to rhodopsin but which are activated by a ligand rather than light
β adrenergic and muscarinic receptors and odorant receptors in the olfactory system
How many G proteins can 1 rhodopsin molecule activate per second?
Each molecule of PDE hydrolyses how many cGMPs?
How many molecules are hydrolyses per photon?
150/s
600 cGMP molecules/ second
10^5 per photon
What percentage of the cyclic nucleotide gated cation channels that are open in the dark are open in light
This blocks the entry of how many cations?
As low as 3%
10^6 cations
What is retinitis pigmentosa (3)
A progressive hereditary retinal degeneration
Gradual onset of night blindness in adolescence, leading to loss of all peripheral vision by adulthood or even total blindness
PDE and the light sensitive channel can also be affected in other cases of hereditary retinal disease
What causes retinitis pigmentosa
No single cause of hereditary RP but 5-10% of cases are caused by mutations in the gene for rhodopsin
What is the dark current
In darkness, when [cGMP] is high, many channels are open and there is a continuous current of Na+ and Ca2+
What is the voltage of a rod or cone when the dark current is circulating
Depolarised to -30mV
What is the outward arm of the circulating dark current
What happens to these channels during illumination
Efflux of K+ in the inner segment
K+ continues to exit through these channels - this results in hyperpolarisation
Is an ion pump needed in rods and cones for the dark current?
A Na/K pump maintains ionic gradients
What happens to photoreceptor channels with flashes of increasing intensity
More and more channels opens causing a graded hyperpolarisation
What is the saturated hyperpolarisation of photoreceptors
When is this reached
How is saturation avoided
-75mV
When all cGMP gated channels are closed
Photoreceptors light adapt by resynthesising cGMP via guanylyl cyclase
What equipment would you use to measure the dark current
Suction electrode
How can you detect single photons
With very dim lights
Define what it means to light adapt
Why would you do this
Reduce sensitivity as the steady light intensity increases
In order to avoid saturation and to allow operation over a wide range of background intensities
What ion mediates photoreceptor light adaptations
What does this ion inhibit which is relevant to light adaptation
Ca2+
Guanylyl cyclase
Describe the regulatory feedback loop of calcium entry by light sensitive channels
In darkness, calcium enters via cyclic nucleotide gated channels, inhibiting GC
When cGMP is reduced by light, the channels close, less calcium enters the cell, but continues to be extruded by a Na/Ca/K exchanger
The resulting drop in calcium relieves the inhibition of GC so more cGMP is synthesised to counteract the effect of excitation
True or false
Rods saturate at relatively high intensities
False
rods saturate at relatively low intensity and vision under photopic conditions is mediated entirely by cones, which can continue adapting under the brightest conditions
How do the basic processes of transduction and adaptation appear to be between rods and cones
The same, with important quantitive differences
What are the quantitive differences between transduction and adaptation in the rods and cones (2)
Cones are 50 times less sensitive than rods and cannot detect single photons
Conal responses are much faster than those of rods
Do rods or cones mediate colour vision
Cones
Colour -Cones (think C)
Define colour vision
The ability to distinguish different objects on the basis of the spectral reflectance independently of their intensity
Each cone absorbs maximally at a particular wavelength. What are the possible wavelengths?
420, 534 or 564nm
Can a single cone be useful for colour vision
Explain
What is this principle
No, alone it provides no colour information
A green: might absorb 10 times fewer read photons than green photons, but 100 incident read photons would nevertheless be indistinguishable from 10 green photons
The principle of univariance
Given the principle of univariance, how is colour vision therefore achieved
By comparing the output of different cones
Describe the trichromatic system
How many colours can it see
Based on 3 cone classes (red, blue, green) with different photopigments
2 million colours
How can we define colour
What theory is this the basis of
By the ratio of excitation in the three current colour classes
Young Helmholz trichrome Theory
Equal excitation of all 3 cones results in what colour
White
What are the commonest cases of hereditary colour blindness
Where either red or green pigment is missing resulting in dichromatic vision
The blue may be missing but this is rare
Describe colour vision in non-primate mammals
Dichromatic, expressing only blue and yellow opsins
How did the red opsin evolve
Why do we think this
By duplication of the green opsin 35 million years ago in Old World Monkeys
Red and green opsin genes share extensive homology (98% identical) and are adjacent on the X chromosome
Because of the proximity of the red and green genes, what can happen
It is not unusual for the DNA strand to align incorrectly resulting in unequal homologous recombination
When this happens between genes (unequal intergenic recombination) loss/ duplication of genes can occur
Or hybrid genes form, which may be functionless, but may form novel rhodopsins with shifted absorption spectra
How can deuteranopia be explained
The absence of the green gene (green-dichromacy)
How can protanopia be explained
Loss of red gene
Red-dichromacy
When do anomalous trichromats emerge
When hybrids are formed with shifted spectra sensitivities
Hence a hybrid green-red gene may give rise to deuteranomaly whereas a red- green hybrid may cause protanomaly
What is tritanopia
Loss of blue pigment
It is v rare
Blue cones are excluded from the fovea, resulting in foveal tritanopia
Blue cones comprise what % of cones
10%
What does the retina contain (6)
photoreceptors four major classes of interneurons: bipolar cells (BC), horizontal cells (HC), amacrine cells (AC) and ganglion cells (GC). There are also glial elements known as Müller cells (MC)
How are the cells in the retina organised
distributed
in five well-defined layers, which can be subdivided into three nuclear layers (containing cell bodies) and two plexiform layers (containing axons and cell processes).
What are the 5 layers of the retina
Outer Nuclear layer Outer plexiform layer inner nuclear layer inner plexiform layer ganglion cell layer
What cells are in each of the layers of the retina
Outer nuclear layer (ONL) - photoreceptor cell bodies.
Outer plexiform layer (OPL) - synapses between photoreceptors, bipolars and horizontal cells.
Inner nuclear layer (INL)- bipolar,
horizontal and amacrine cell bodies
Inner plexiform layer
(IPL) - synapses
between bipolar, amacrine and
ganglion cells.
Ganglion cell layer (GCL)- cell bodies of
ganglion cells.
What is the direction of information flow in the retinal layers?
What are the neurotransmitters involved?
from photoreceptors to bipolar cells (IB/FB)
to ganglion cells (G).
All of these cells use glutamate as neurotransmitter
Which cells mediate lateral inhibition in the retina
Which NT is used
horizontal cells
GABA
What are amacrine cells? What are they used for and where are they found?
mediate a diverse collection of interactions in the inner retina, and use many different transmitters.
Which cells photoreceptors synapse with?
ONLY with bipolar cells and horizontal cells
What cells do ganglion cells in the retina receive input from
bipolar and amacrine cells
Which cells mediate the output of the retina
carried by the axons of ganglion cells which together form the optic nerve
Do retinal neurons use action potentials?
Most retinal neurons use graded potentials.
Only ganglion cells use action potentials, whilst amacrine cells usually only fire spikes in response to strong stimuli
Why are graded potentials used in the retina and not action potentials
they are a more efficient means of transmitting information over short distances
Does the retina exhibit divergence or convergence
both divergence (for parallel processing) and by convergence (for spatial summation).
Overall, exhibits convergence,
possessing 6 million cones, 120 million rods, but only 1.5 million ganglion cells.
Where is the highest resolution on the retina
Does convergence or divergence take place here
fovea
there are ~3x more ganglion
cells than cones (net divergence)
Describe how the cells of the peripheral retina reflect its lower resolution
there is only one ganglion cell for every ~16 cones (net convergence and loss of spatial information).
What is characteristic of the photoreceptor synapses in the retina
presynaptic ribbon
What is the presynaptic ribbon characteristic of photoreceptor synapses
a modified presynaptic
density characteristic of synapses that
transmit graded signals.
Why is the term synaptic triad used when discussing photoreceptor synapses
The postsynaptic targets always include processes from both bipolar and horizontal cells
Describe the synapse of cones in the eye (2)
Cone terminals end in a large synaptic
swelling - the cone pedicle.
Cones form both invaginating
and flat synaptic contacts
How many synapses can be associated with 1 cone pedicle
What does this reflect
up to 30
divergence of the cone signal to numerous bipolar cells
Describe the synapse of rod synaptic terminals
called spherules
smaller than cones - only 1 synapse per rod (ie no divergence)
How many rods can lead into 1 bipolar cell
many
indicates convergence and a loss of spatial resolution
Define the receptive field of a visual cell
the area on the retina (or its projection in the visual field) from which its activity can be influenced by light.
What is the purpose of a receptive field
serves to define the position of a stimulus within the
retina, while its size corresponds to the degree
of convergence.
What does a visual cell’s receptive field usually contain
both excitatory and
inhibitory regions. Different spatial regions
of the receptive field may also differ in their
sensitivity, for example to wavelength.
What kind of receptive field is typical of a retinal neuron
centre surround, with a circular receptive field centre and a concentric surrounding annulus
Illumination of the receptive field centre and the surround have antagonistic effects on the cell’s overall response.
What is the effect of illumination of an on-centre receptive field
excited by light in the central region and inhibited by illumination of the surrounding annulus.
How does illumination affect an off-centre receptive field
inhibited by illumination of the centre and excited by the surround.
What provides the lateral inhibition in the retina
centre surround antagonism
What does subdivision into on and off centre receptive pathways
allows the localisation of bright and dark regions of the visual image.
How do synaptic interactions at the cone pedicle interact with bipolar cells
Synaptic interactions at the cone pedicle establish an antagonistic, centre-surround receptive field structure in the bipolar cells.
Each cone contacts numerous different classes of bipolar cell, including both “on-centre” and “off-centre” cells.
How does the membrane potential of bipolar cells change with stimulation
Off-centre bipolar cells hyperpolarize, like the photoreceptor, to a “centre” stimulus, but depolarize to a “surround”
On-centre bipolar cells respond in the opposite way, depolarizing to a centre stimulus, via a metabotropic glutamate receptor (mGluR6)
What is released on to off centre bipolar cells in the retina during darkness
What happens when the cone is illuminated
In the dark the
cone continually releases glutamate which depolarizes the bipolar
cell by opening cation channels (ionotropic glutamate receptors).
it hyperpolarizes, transmitter
release is reduced and therefore the bipolar cell also hyperpolarizes.
How does the structure of horizontal cells reflect their function of using many cones for lateral inhibition
have broad dendritic fields, collecting inputs from a large number of cones, and which form inhibitory feedback synapses back onto the photoreceptors.
How does the membrane potential of horizontal cells change in light
What does this mean
hyperpolarise
therefore when only the surround is stimulated the central photoreceptor (now not illuminated) will
depolarise (as it receives less inhibition from
horizontal cell feedback)
What does activation of a on centre bipolar cell mGluR6 lead to
Like rhodopsin, this
activates a G protein resulting in the closure of cation channels in response to photoreceptor transmitter release in darkness (a sign-inverting synapse)
How do we think bipolar mGluR6 GPCR cascade works
Details of the
transduction cascade are unclear, but it may
operate via direct inhibition of the cation channel by
the G protein α subunit
How does light affect the on-centre bipolar cell
When light
hyperpolarises the photoreceptor, thereby
decreasing transmitter release, inhibition is relieved and the channels open, so the on-centre bipolar cell depolarizes.
True or false
Every cone contacts both on- and off-centre bipolar cells.
true
each cone contacts 2 different classes of bipolar cells
Every cone contacts both on- and off-centre bipolar cells. How does the synapse differ for different connections
Sign-inverting synapses to on-centre bipolar cells are formed at the invaginating contacts, using metabotropic mGluR6 receptors. Sign-preserving synapses
to off-centre bipolar cells correspond to flat contacts, using ionotropic AMPA receptors.
describe sign inverting synapses to on-centre bipolar cells
formed at invaginating contacts using mGluR6
Describe sign perserving synapses to off-centre bipolar cells
correspond to flat contacts using ionotropic AMPAr
What kind of bipolar cells are most common in primate eyes
Give 3 facts about this type
midget bipolar cells
receive input from just one cone
have small receptive fields
colour specific signals
What is the benefit of midget bipolar cells receiving input from just one cone
small receptive field so have the potential to signal the finest spatial detail in the image
describe the 2nd type of bipolar cells (not midget) (3)
Diffuse bipolar cells have larger receptive fields,
collect input from 5-10 cones.
Convergence
means that their responses are more sensitive,
but spatial detail and colour signals are lost
Are bipolar cell types specific to either on or off centre fields?
Both diffuse and midget bipolar cells come in on- and off-centre classes.
How many bipolar cells does each cone contact in the fovea?
Which class?
What is this intended to do ?
a each cone contacts 10-15 bipolar cells of different classes.
This divergence is
the first step in establishing parallel streams in the visual system
What are the parallel streams in the visual system
different aspects of the
image are coded by different cells with
overlapping receptive fields. Thus the
message conveyed to the brain consists of
parallel “neural images”, each specialised for
a different aspect of the image - such as onvs off-, spatial detail, temporal detail or
colour
What is the first step in establishing parallel stream processing in the visual system
The divergence in the fovea of each cone contacting 10-15 bipolar cells of different classes.
What is the effect of convergence in the visual system
while it increases
sensitivity, sacrifices spatial resolution by pooling photoreceptor signals
Do rods and cones connect to the same bipolar cells
no
diffuse and midget bipolar cells receive direct input exclusively from cones
an anatomically and functionally distinct rod bipolar cell receives direct input from rods.
Are the bipolar-to-ganglion cell synapses excitatory or inhibitory?
What does this mean for the receptive field structure of ganglion cells
excitatory
consequently the ganglion cells have a similar receptive field structure to bipolar cells
Which cells modify the bipolar-to-ganglion cell synapses
lateral interactions from amacrine cells.
What is important about the balance between centre and surround in inner retina cells
The approximate balance between centre and
surround is the important parameter for such
cells, and over a wide range of ambient
intensities they maintain a similar receptive
field structure, responding to increments or
decrements of intensity in the appropriate part
of their receptive field
Why does diffuse light give a weak response from centre surround cells
An on-centre cell will respond when a light turned on in the centre of its field, or when a light is turned off in its surround.
A diffuse light covers both excitatory and inhibitory regions, which cancel each other out, leaving at most only a weak response.
What is the point of lateral inhibition within centre surround receptive fields
to emphasise contrast borders in the visual image.
The antagonistic
surround effectively subtracts a signal
proportional to the mean background.
Why is the centre surround system a very economical way of encoding an image
How does this system also contribute to adaptation in a way
because it rejects redundant information
helps to prevent
saturation as the ambient intensity increases
What is the most important way to subdivide primate ganglion cells
What are the proportions of each in the retina
into magnocellular (20%) and parvocellular (80%) classes
Are magnocellular and parvocellular classes on or off centre
both these classes come in “on” and “off” centre cells
What are midget ganglion cells
another name for parvocellular cells
Describe the structure of parvocellular ganglion cells
small dendritic fields
collects information from only 1 cone via 1 midget bipolar cell in the fovea
Describe the centre surround structure of parvocellular ganglion cells
one colour in the centre and another in surround
eg centre might be driven by a red cone and the surround antagonistically by green or vice versa
can be off or on centre
if the centre of the receptive field of a parvocellular ganglion cell is blue what will the surround be?
yellow (driven by both green and red cones to make yellow)
What is another name for magnocellular ganglion cells
parasol ganglion cells
What is the structure of magnocellular ganglion cells?
What is the input from
larger dendritic fields and large diameter axons
collect input (central) from many photoreceptors -
including both R and G cones - via diffuse
bipolar cells
How do magnocellular ganglion cell function differ from that of parvocellular? (4)
magnocellular respond more rapidly, and
generate transient responses to step changes in contrast.
more sensitive than P cells and have larger diameter axons (faster
conduction velocity).
Where do parvo and magnocellular ganglion cells project to
distinct layers in the LGN and cortex, which appear to
be specialised for detection and processing of
motion stimuli
Which are the most morphologically diverse retinal cells
How diverse are they
amacrine cells with as many as ~50 distinct classes, using numerous different neurotransmitters
We know relatively little about different functions of amacrine cells. What do we know about some of them? (3)
Some have extensive dendritic fields and are likely to supplement the horizontal cells in contributing to inhibitory surrounds by feedback at both bipolar and ganglion cell level.
Others are likely to be involved in modulatory functions, such as the role of the dopaminergic amacrine cell in adjusting the eye for photopic and scotopic vision
The rod, or AII amacrine cell, mediates the signals from rods under scotopic conditions.
Is the input from amacrine cells evenly distributed between parvo and magnocellular ganglion cells?
no
M ganglion cells receive significantly
more amacrine input than the P cells
M ganglion cells receive significantly
more amacrine input than the P cells. What might this contribute to
their transient response properties
What is rod pooling and what does it result in
convergence of rod signals
sacrifices spatial resolution for extra sensitivity
What is Purkinje shift
overall spectral sensitivity is shifted from ~560 nm (the average peak sensitivity of the
red and green cones) to the rod peak
sensitivity of ~500 nm
What is the pathway of information flow from the rods in the fully dark adapted retina
rod-> rod bipolar cell-> rod AII amacrine cells -> activates ‘on centre’ cone bipolar cells and inhibits ‘off’ bipolar cells -> ‘on’ ganglion cells
What feature of the rod pathway allows sensitivity at low luminance? (2)
massive convergence in this
pathway:
(~1500 rods > 100 rod-bipolars > 5 AII amacrines > 4 cone bipolars> 1 ganglion
cell);
together with the rod’s ability to detect single photons
is the rod pathway at twilight the same as in the fully dark adapted retina
no
alternative simpler route involves electrical synapses from rod spherules directly to cone pedicles. The rod signals thereby hijack the cone pathway at mesopic intensities when both rods and cones can function.
When activated by rod bipolars in the fully dark adapted retina, how do AII amacrines interact with cone bipolars
connect via gap-junctions to “on centre” cone bipolar cells which transmit the signal to “on” ganglion cells in the usual way. The same AII amacrine cell makes inhibitory (glycinergic) synapses with “off” bipolar cells.
How can the optic nerve be considered in the visual system
a bottleneck
In what way is the optic nerve a bottleneck in the visual system
over 100 million photoreceptors condensed into the axons of 1.5 million ganglion cells.
How many neurons are in the primary visual cortex?
What does this reflect
200 million
The sophistication of neural processing in the cortex is reflected in this overall massive divergence
Where is the primary projection from the retina to?
Do any of the ganglion cells project elsewhere?
LGN in the thalamus
10% project to other areas eg pretectum, suprachiasmatic nucleus and superior colliculus
what are the following destinations of visual ganglion cells involved in:
pretectum
suprachiasmatic nucleus
superior colliculus
pretectum - for pupillary responses,
suprachiasmatic nucleus - circadian rhythms
the superior colliculus (involved in eye movements).
Fibres from which parts of the retina go to the right LGN
fibres from the nasal retina of the left eye and temporal retina of right eye project, via the right optic tract
What do the fibres from the LGN do
fan out in the optic radiation through the internal capsule, ending in the primary visual cortex at the occipital pole
What is the primary visual cortex also known as
V1 or striate cortex
Where is V1 found anatomically
largely buried
in the medial aspect of the hemispheres, in the calcarine sulcus
What would it mean to say the regions surrounding V1 form a retinotopic map?
What is an excception
an orderly point-for-point representation of the retina is maintained
fovea is overrepresented (cortical magnification)
What does the LGN consist of?
What is the input
4 parvocellular layers (receiving input from P ganglion cells) and 2 magnocellular (input from M ganglion cells)
each layer receives input from only 1 eye and 1 of the 2 classes of ganglion cells
koniocellular layers are located between each of layers 1-6
What do the koniocellular layers of the LGN contain
very small cell bodies that receive input from blue cone ganglion cells
How can the LGN be consider a relay station
Is this the whole truth?
ganglion cell axons make direct excitatory connections with LGN cells which then project directly to the cortex
no: there are also local interneurons and about 30% of the synaptic input to the LGN comes from feedback pathways from the cortex.
How thick is the grey matter of the visual cortex?
How can it be divided
2mm
into 6 layers
Where do fibres from the LGN end in the primary visual cortex
on spiny stellate neurons in
layer 4.
What are the different parts of the visual cortex that magno- and parvocellular inputs project to
distinct sublaminae of layer 4 (4C-alpha and 4C-beta respectively)
Which layers of the visual cortex give output to higher visual areas
primarily from pyramidal cells in layers 2 and 3
What do the different layers of the visual cortex do?
1? 2 and 3: output to higher visual areas 4: input from LGN 5: project to deep brain structures such as superior colliculus 6: projections nack to the thalamus
How do the receptive fields of the LGN differ from the cells in V1
LGN: similar to ganglion cells with centre surround organisation
V1: orientation tuned
What are the 2 broad classes of orientation tuned cells in V1
simple and complex cells
Describe simple orientation tuned cells in V1
respond only to an edge of a particular
orientation in a very well-defined position.
The receptive field has an inhibitory flank on
one or both sides, and with diffuse
illumination excitation and inhibition cancel.
Where are simple cells common in V1
in input areas ie layers 4 and 6
What % of V1 orientation tuned cells in V1 are complex cells
75%
mainly in layers 2, 3 and 5
What do complex orientation tuned cells in V1 respond to
respond best to oriented bars or edges, but position is not so critical. They respond hardly at all to spots or stationary patterns, and best to moving edges over a somewhat larger visual field. They are often directionally selective
What are hypercomplex orientation tuned cells
Some simple and complex cells respond only to short bars, becoming inhibited when the edge exceeds a critical length. Such cells are now said to exhibit end-stopping or end
inhibition
What did Hubel and Wiesel speculate
that a simple cell receptive field might be generated by combining inputs from several appropriately aligned on and off centre LGN inputs.
How might the complex cell receptive field be generated
by summing together the outputs of a few appropriately arranged simple cells, adding also some circuitry for detecting motion.
How can you study the arrangement of orientation tuned cells in the V1 cortex
What do results show?
by examining the preferred orientations of the cells encountered during an electrode penetration.
When the electrode passes perpendicular to the cortical surface, all the cells show the
same orientation preference.
But when the electrode penetrates the cortex obliquely, there is an orderly progression of preferred orientation along the electrode track.
How are orientation tuned cells arranged in V1 (3)
cells of similar orientation tuning are organised in orientation columns perpendicular to the
cortical surface.
Adjacent columns have only slightly differing orientation preferences.
All orientations are represented over a distance of ~1.0 mm in an orderly progression
True or false
Because of the partial decussation at the optic chiasm, each half of the brain recieves input from the ipsilateral visual hemifield
False
each half of the brain
receives input from the contralateral visual
hemifield
What happens if you inject one eye with titrated proline
the label is taken up by ganglion cells and transported via the LGN to the visual cortex, revealing the pattern of afferent termination within layer 4c. It is distributed in labelled patches which receive input from the injected
eye, separated by unlabelled regions which receive input from the other eye
How wide are the ocular dominance columns in the visual cortex
How are they arranged
0.5mm wide
alternating columns receiving input from one eye then the other
in 4C ocular dominance is complete but is more balanced between both eyes in other layers
If a V1 neuron receives input from both eyes, how does the receptive field from each eye compare?
Usually have receptive fields locate at corresponding positions on the two retina
sometimes respond to stimuli at different positions on either retinae - disparity detectors
What is a disparity detector
if a neuron receives input from both eyes but its receptive fields correlate to different points on either retina they can detect objects nearer or further than the plane of fixation
used in stereopsis
What is stereopsis
When is this important
What does it use
the binocular judgement of relative depth.
This is especially important when judging the shape of complex objects.
disparity detector
How can we detect the parts of V1 involved in colour processing
staining for cytochrome oxidase - reveals blobs in the middle of each ocular dominance column with unstained interblob regions
Are cells within the blobs of the primary visual cortex orientation tuned?
no - show centre surround anatagonism which respond selectively to particular wavelengths and are involved in processing of colour
What is a hypercolumn in the primary visual cortex
a 1-2mm^2 region representing a small region of visual space, in which all orientations are represented, and
which contains both left and right eye ocular dominance columns each with a blob for colour analysis.
therefore contains all the cortical machinery necessary to analyse this small region of the image
How do receptive fields vary within each hypercolumn in V1`
vary in size, typically with the finest detail in 4C and layer 3, with larger fields in layers 5 & 6.
What is each area of space analyzed with respect to in V1 (6)
each area of visual space is simultaneously analysed in V1 by ~105-106 neurons with respect to: contrast, orientation, length of line elements, direction of movement, spatial grain, colour
What is teh columnar structure of V1 like in real life?
ocular dominance: tiger stripe pattern
orientation columns: orientation pinwheels
What is the orientation pinwheel arrangement in V1
where orientation columns are arranged radially around a central hub.
How can the actual layout of orientation columns and ocular dominance columns be visualised?
intrinsic imaging of cortical activity
When are Ocular dominance columns and orientation tuning established
during a critical period
of neonatal development (3-5 weeks in
kittens, 1-2 years in humans)
What happens if you monocularly deprive a kitten in 3-5 weeks of neonatal development
cells in the primary visual cortex come to be dominated by input from the unoccluded eye
(this is the time when the hypercolumns are established)
What happens if you raise a kitten in an environment containing only vertical stripes
Can this be corrected later in life?
most cells in V1 will be tuned to vertical bars
no
What can cause amblyopia
how common is this
a visual problem in early life such as an uncorrected squint, astigmatism, or wearing an eyepatch
this defect will be permanent
5% of population
What is amblyopia
a permanent visual defect in cortical function
How many higher visual areas have been identified
How are they often simplified
30+
each to some extent specialised to a particular function
the dorsal “where” pathway which is dominated by cells of the magnocellular pathway, and the ventral “what” pathway which has mainly parvocellular input.
Which cells dominate the where and what pathways in higher visual processing
where: magnocellular
what: parvocellular
What is V2 and hwo does it anatomically relate to V1
The first visual assocation area
directly adjoins V1.
How can V2 be subdivided with cytochrome oxidase staining
into thick and thin dark stripes and pale interstripes.
Where does area V4 receive input from
the thin stripes and interstripes of V2
What are the 2 parallel systems in V4
a parvo - blob - thin stripe - V4 stream
which is particularly concerned with colour
and
a parvo/magno - interblob - interstripe
- V4 stream concerned with edges and analysis of fine form.
Which area detects the illusory contours of Kaniza’s triangle
V2
What do lesions in V4 lead to
achromatopsia (cortical colour blindness)
What are the final destinations of the parvo-magno stream in V4 (stream concerned with edges)
the inferotemporal (IT) cortex where
some of the most highly sophisticated cells
have been found, responding for example to
faces and hands
What happens if you damage the parvo-magno stream of V4?
What other damage can lead to this
inability to recognise faces (prosopagnosia)
damage to the inferotemporal cortex
What is the pathway of the magnocellular input into V1
into layer 4C-alpha to layer 4B -> thick stripes of V2-> V5 and V5a -> posterior parietal cortex (Some of the output destinations of MT include brain stem nuclei controlling eye movements)
What are areas V5 and V5a also known as
MT and MST
What dominates all levels of the dorsal ‘where’ pathway of visual processing
dominated by rapidly
responding, movement detecting cells with little colour preference.
Cells in the dorsal ‘where’ pathway in visual processing have little colour preference. What do they respond to?
movement
binocular depth cues
Cells in MST show sophisticated response selectivity, responding to motion illusions and flowfields
What do the cells in MST area involved in the dorsal visual where pathway show response to
show sophisticated response selectivity, responding to motion illusions and flowfields
What are flow fields
whole field patterns of movement
normally generated by the motion of the eyes,
head or body through space
What does a lesion in MT lead to
inability to see movement
How much binocular overlap is there in humans
extensive overlap
with forward facing eyes, yielding a large region for stereopsis
Do non primate animals usually have good binocular vision
with laterally-facing eyes, the degree of
overlap is more limited, yielding a larger visual field but less overlap
Compare the visual field and overlap of humans and dogs
the visual field of
each eye is similar (150º) in dogs and
humans, but the binocular overlap is reduced
(60º versus 120º) expanding the field of view
How does the binocular overlap of cats compare to humans
cats have forward-facing eyes, and a similar degree of binocular overlap to humans
Other than position of the eyes on the head, what else affects he visual perspective of an animal
height of the animal
there would be little
advantage to a very small animal such as a mouse or rat to accommodate at infinity!
True or false
all animals have foveas
false
Most non-primate mammals do not have a fovea, but instead have a visual streak with increased photoreceptor (and ganglion cell) density to image the horizon
What is the ultimate purpose of colour vision
to allow the detection of objects which reflect light of different spectral composition from the backgrounds upon which they are superimposed.
Do perceived colours of objects depend on illumination?
ideally not - visual system should estimate the spectral reflectance of objects, irrespective of the spectral composition of the illuminating light
What is the range of wavelengths human colour vision can respond to
from 400 nm at the blue end of the spectrum, through 500 nm in the green, to 700 nm in the far red
What is human colour vision based upon
absorption of light by three different cone
pigments, which preferentially absorb at short, medium and long wavelengths.
(each cone only has 1 pigment)
What is the response of colour sensitive cones initiated by
the absorption of light by the photopigment, which determines the action spectrum of the cone
Will one wavelength stimulate more than 1 cone?
yes
The pigment absorbance curves are quite broad leading to significant overlap,
especially between the medium and long pigments
What is spectral univariance?
receptor cell can be excited by different combinations of wavelength and intensity, so that the brain cannot know the color of a certain point of the retinal image.
What does the possesion of more than 1 cone class allow
allows discrimination of objects which differ in colour but not intensity.
Suppose that a monochromat, views an object reflecting a single wavelength superimposed on a background of equal intensity and a different wavelength. What happens if the object causes the same cone response as the background?
How would a dichromat improve on this?
it will be indistinguishable
can discriminate them as this object preferentially stimulates short wavelength cones, whereas the background preferentially stimulates long wavelength cones.
How is colour discrimination determined
comparing the degree of stimulation of the different cone classes.
Describe a graph to describe colour spectrum for a dichromat
What is the colour line on this graph
How is the colour that is stimulated represented?
y axis= green (M)
x = red (L)
a vector passes through origin and the line’s length represents brightness while its angle to the axes indicates colour
As the wavelength becomes progressively longer, the vector pivots from y towards x
In between, both cone types are stimulated, giving rise to yellow
colour line= d the line joining the
100% stimulation points on the two axes
the intersection between the vector and colour line
What about the anatomy of the eye allows the graded response to colour represented by the graph which in a dicchromat has % green on y and % red on x?
The overlap between the pigment curves is
vital for this graded response to wavelength:
narrow non-overlapping pigment spectra
could not give rise to such a graded response.
How is the graph which in a dicchromat has % green on y and % red on x adapted to trichromats?
what does this alloww construction of
extended to 3D, with R,G,B on x, y, and Z axes respectively
colour triangle
Describe the colour triangle
equilateral triangle with B, G , and R at each vertex
centre represents white
a curve passes up the blue side curves across the interior, cutting off the green vertex, to join the R side
As the wavelength becomes longer response point moves from B
vertex along the curve to R vertex
unattainable region at G vertex
Why is there an unattainable region at G vertex
where all three classes are being excited
Cone responses combine information
about brightness and colour. How does the visual system transform this?
into independent colour opponent channels
What is the red-green opponent channel in the visual system
the signal is the difference between the responses of the medium and long wavelength cones
What is the blue yellow opponent channel in the visual system
formed from the difference between the responses of the
short wavelength cones, and the sum of the medium and long wavelength cone responses.
How can the visual system use colour opponency channels to represent luminance
By summing together the responses of the
medium and long wavelength cones
How do the colour opponency channels give a high sensitivity to changes in wavelength
produce a steep variation of response with wavelength in the regions of pigment curve overlap
How do the colour opponency channels correspond to the colour triangle (5)
correspond
to a transformation of co-ordinates in the triangle.
point at the centre
represents white, when all three cone classes are stimulated equally.
Crossing this point are 2 colour opponent axes.
horizontal axis represents the differential excitation of red vs green cones;
the vertical axis
represents the differential excitation of blue cones versus red and green cones.
What classes do most retinal ganglion cells in terms of colour
fall into red-green and blue- yellow antagonistic classes.
What are single opponent cells
colour coded ganglion cell where center is excited by one colour (eg red) and the surround in inhibited by its opposite (eg green)
Why are single opponent ganglion cells called this
the antagonism takes between different regions of the receptive field, driven by different cone mechanisms
Which type (M or P) do single opponent ganglion cells correspond to?
Hence where do they project to
Is this true of all single opponent ganglion cells?
P cells
project via the parvocellular layers of the LGN
blue-yellow opponent signals
originate in small bistratified ganglion cells and pass to the LGN via a distinct
koniocellular pathway
What are broad band ganglion cells?
driven by both red and green cones. They exhibit centre surround
antagonism without a chromatic component,
thus encoding luminance
Which class of ganglion cell (M or P) do broad band ganglion cells correspond to?
Therefore where do they project to
M cells
project via the magnocellular layers of the LGN.
What are non concentric ganglion cells
do not exhibit centre-surround antagonism.
receptive fields may be driven by one or several cone classes, without antagonism.
Why are single opponent cells flawed?
Use an example to explain this
How is this solved?
ambiguous for colour and brightness
a red-green single opponent cell cannot discriminate between large and small red spots and a small white spot
double opponent receptive fields where chromatic antagonism takes place not only
between centre and surround but also within each region.
Give an example of double opponent receptive field
red light might
excite the centre and inhibit the surround, whereas green light would inhibit the centre and excite the surround.
Where are double opponent cells found
cytochrome oxidase blobs of the striate
cortex, which receive inputs from the parvocellular and koniocellular layers of the LGN
What are interblob regions of the striate cortex used for
analysing spatial form and motion
How are double opponent receptive fields constructed
by antagonistically connecting together single opponent cells of opposite
colour preference at appropriate positions on the retina.
What does antagonistically connecting
together single opponent cells of opposite colour preference at appropriate positions on the retina result in?
double opponency receptive fields
lower spatial resolution of the colour signal
Where do the neurons with double opponent receptive fields project to?
How do cells in this region respond?
via the thin stripes to V4 in area
18.
cells in V4 exhibit a very narrow degree of spectral tuning, each responding only to a narrow band of wavelengths
What do the cells in V4 represent in terms of colour analysis?
no longer represents the opponent channels seen lower down the pathway, but deals instead with individual colours or hues.
These properties contribute to the
phenomenon of colour constancy
Is any of the interblob region involved in colour processing
yes
A subset of simple and complex cells in the interblob region respond best to coloured edges. This allows the boundaries between different coloured regions to be detected.
What can a trichromat do in a Rayleigh match?
can always match a test light of
arbitrary colour by appropriately adjusting the
intensities of three primary colours in a
Rayleigh match.
How do you set up a Rayleigh match
primaries must be reasonably well spaced in wavelength, so as to preferentially
stimulate each of the classes of cone.
In the simplest form of match it is simply necessary
to adjust the relative intensities of our 3 primaries on one side of the screen in order to match the test light, L, on the other.
However, sometimes necessary to add 1 of 3 primaries to the same side of the screen as L, because L may not sufficiently stimulate one of the cone classes.
What are the human colour vision abnormalities involving only one cone class?
What do they all lead to
protanopia (red),
deuteranopia (green), or
tritanopia (blue)
dichromatic vision
what is protanomaly
Red cone pigment is shifted towards yellow, meaning that more red is needed in colour matches than for a
normal observer in order to sufficiently
stimulate this abnormal pigment with a shorter than normal peak wavelength
What is deuteranomaly
the green cone pigment is shifted towards yellow, with an equivalent need for extra green in the colour match.
How common are congenital colour anomalies
green-red: relatively common
blue: very rare
What is tritanomaly
congenital abnormality of the blue mechanis
very rare
are colour opponent cells responsible for colour opponency within or between objects
mainly within an object’s boundaries
double opponent cells can
also enhance colour contrasts across the
boundaries of object
Give an example of how we correct for the variations in the spectral composition of the illuminating light and thereby aid a more accurate assessment of reflectance.
Suppose that a colour-encoded cortical cell preferentially responds to red light. If a Mondrian is illuminated with red light then such a cell in Area V1 will respond to red light reflected within its receptive field, irrespective of the spectral reflectance (or “colour”) of the patch.
However such a cell in V4 will only respond to red light reflected from a red patch, but will not respond to light reflected from a neighbouring patch of another colour.
the red patch reflects a larger proportion of the red light than surrounding patches of other colours, while neighbouring patches of other colours reflect a smaller proportion of the red light than does the red patch and are therefore inferred to have a different spectral reflectance
What does colour constancy in V4 involve
involves comparisons across large areas of the visual field
What is the range of intensities humans can see
from just a few photons to 10^15 times brighter than that (if it gets much more intense than this, vision ceases and retinal damage results)
What is the first factor that allows such an enormous range of intensities to be seen
use of both rods and cones in a duplex retina.
What is the range of rod detection of intensity
extremely sensitive so that they can
respond to light of very low intensity within the scotopic range
In what part of the retina is scotopic sensitivity highest
How is this reflected in the cells present
parafoveal region (highest rod density)
What happens to the retinal cells as the intensity starts to increase beyond the scotopic range
the less sensitive cones start to
respond too within the mesopic range.
What happens to cell response in the retina as intensity increases beyond mesopic range
intensity is too high for rods, whose responses saturate, so within the photopic range only the cones contribute.
Does the eye need to function over the full range possible?
At any instant the eye only receives a much smaller range of intensities, because objects normally reflect light from some other light source in proportion to the reflectance of the
object.
What is the intensity range the eye actually needs to operate over
10^2 - 10^3
Is the visual system concerned with absolute intensities?
no but instead with the differing reflectances of objects, according to whether
they are at the top or the bottom of the current operating intensity range.
How can adaptation be subdivided
field (or light) adaptation
bleaching adaption
Describe field adaptation
also known as light
adaptation, is the rapid and reversible change in sensitivity which takes place when the steady intensity is altered
What is bleaching adaptation
the profound decrease in sensitivity induced by very bright light, which recovers only slowly thereafter upon dark adaptation.
How can field adaptation be investigated
increment-threshold experimentation
Describe increment-threshold experiments for light adaptation
sensitivity of the rod system alone is tested using a stimulus consisting of a green test
spot, which preferentially stimulates rods, superimposed on an orange background,
which preferentially adapts the medium and long wavelength cones.
The subject fixates on the eccentrically-placed cross, so that the stimulus falls on the parafoveal region where the rod density is highest.
The experiment consists of determining the threshold test spot intensity as a function of steady background intensity
How does delta I change with background intensity in the increment threshold experiment
Over a wide range of intensities the log of the threshold intensity, delta I, increases linearly with the log of the background intensity, I, the
slope of one indicating that the threshold is
directly proportional to the intensity of the background.
Describe threshold intensity at v low intensities
threshold is independent of background
intensity.
This absolute threshold in darkness is set by an internal signal similar to background light, known as the dark light
Explain Webber’s law
If the dark light, I0, is added to the actual
background intensity, it allows the form of the
entire curve to be explained.
Within the Weber
range of intensities, delta I/I is constant; this ratio is the threshold contrast.
How does Weber’s law apply to rods and cones
When the background becomes very bright, the rod system saturates, resulting in a steep increase in threshold with background intensity. Under normal conditions, when the rod system is not artificially isolated by this stimulus, the less sensitive cone system takes over well before rod saturation, and exhibits its own Weber law adaptation.
How will responses change in rods to flashes of increasingly brighter light? Compare between this being done in steady light and in darkness
During background light the response to a given flash is smaller than in darkness: the rod has adapted to the background according to Weber’s law (become less sensitive)
rod responses also become faster
What does the fact that rod responses to flashes of increasingly intense light become faster?
Is the same effect seen in cones
photoreceptors are able to
respond to more rapid changes in bright light
than in dim light.
Similar light adaptation also
takes place in cone photoreceptors
Which second messenger molecule is controlled in photoreceptor light adaptation
cGMP
How do levels of ions change in photoreceptors when light hits the receptor
cascade leads to decreased [cGMP] and closure of ion channels in outer membrane
this stops Ca2+ and Na+ entering the outer segment
the Ca2+ that enters is pumped out by NCX.
When Ca2+ influx
decreases in the light, this efflux continues for a while, so the [Ca2+] falls. This drop is important in light adaptation
What is the most telling evidence for {ca2+] influencing light adaptation
when the fall in [Ca2+] is
prevented, light adaptation is abolished also,
and the receptor saturates at a relatively low
intensity
How does Ca2+ act on the light transduction pathway (3)
Give effects in light
inhibits GC
so in light, when [Ca2+] falls, inhibition is relieved and [cGMP] increases
Ca2+ prolongs activation of photoisomerised rhodopsin
Thus activation switches off more rapidly when the [Ca2+] falls during illumination
Also affects affinity of cGMP activated channel
Why is the rate of destruction of cGMP by PDE important for light adaptation
by allowing changes in cGMP concentration to follow changes
in PDE activity more closely
How does light adaptation of an individual rod differ from adaptation of the entire rod system
adaptation in rods takes place at higher intensities than the whole system, which acts only to prevent saturation in the mesopic range
How are rods connected
converge to form an adaptation pool
rod convergence provides both a visual signal and a signal for adaptation
What does the adaptation pools allow
adaptation of the rod system to take place within the retina, somewhere between the receptors and the ganglion cells.
how is the adaptation of the rod system demonstrated to by between receptors and ganglion cells
How does this work
by the curve shifting of
individual ganglion cells as the steady
background intensity increases.
appears to involves changes in the way in which the rod signals are summed together.
One possibility is that it may take place at the
photoreceptor-bipolar cell synapse
Is light continuous
no is composed of quanta
What are quantal fluctuations in terms of photoreceptors
When the light is extremely dim, the rod only occasionally absorbs a photon, yielding distinct responses. As the light becomes brighter, these individual events merge together, to give a response which displays quantal fluctuations because of the random arrival of individual photons.
How do quantal fluctuations change as light becomes brighter
the size of
the fluctuations decreases because the larger
the number of photons, the smaller the
fluctuation in comparison with the mean:
fluctuation is proportional to sqrt I
and mean is proportional to I
Why must the eye consider quantal fluctuations?
How do these fluctuations affect the visual system
How can this be revealed experimentally
During dim steady light, any stimulus must be detected as being distinct from these random fluctuations.
limit the sensitivity of the system
by repeating the increment-threshold experiment with a small stimulus presented for a short time which will thus deliver only a few quanta to a small number of rods.
designed to maximise the effect of quantal fluctuations.
Dedscribe the fluctuations limit threshold in the human visual system
At very low intensities, the sensitivity is limited by the dark light, as before. At higher intensities, the curve rises according to
Weber’s law, and ultimately saturates. But at intermediate intensities, the curve rises more
shallowly than Weber’s law, with a slope of 0.5 which corresponds to a square root relationship between the threshold and the background intensity. This indicates that the response must be bigger than the fluctuation
in order to be detected.
True or false
In darkness the rod system is free of fluctuations
false
rhodopsin can spontaneously isomerise due to thermal agitation
What happens if rhodopsin spontaneously isomerises during darkness
spontaneous isomerisation every
couple of minutes in any given rod - spontaneous quantal events
What sets the absolute threshold for scotopic rod vision
spontaneous quantal events are believed to cause the dark light in the retina
What happens if a human subject views a very bright light and then returns to darkness
What does this depend upon
What is this process therefore called
visual sensitivity it greatly decreased
not only on light’s intensity but instead on total amount of photopigment bleached during
the light exposure
bleaching adaptation
After bleaching adaptation, how does sensitivity to the darkness return
via dark adaptation
How does dark adaptation vary between using a bright white stimulus and a small red stimulus to only foveal cones?
white - both rods and cones stimulated so sensitivity returns in 2 stages
red: only first component of this recovery is seen
How does light adaptation in a rod monochromat differ from in a normal human
What does this information tell us
the first component of recovery is absent
first component is due to the
rapid recovery of cones, and the second due to
the slower recovery of the rods
In dark adaptation, the first component is due to the
rapid recovery of cones, and the second due to
the slower recovery of the rods. What is the division between these phases called?
rod-cone break
Does spectral sensitivity change in dark adaptation
yes progressively changes in the purkinje shift
Before the rod-cone break, vision relies on middle and long wavelength cones and the threshold is lowest at 550 nm.
But later when the rods take over, the
wavelength of peak sensitivity changes to the peak wavelength of rhodopsin at 500 nm.
How much rhodopsin has recovered from bleaching during dark adaptation by the rod-cone break?
90%
By the time of the rod-cone break, the regeneration of rhodopsin is more than 90%
complete. What is the sensitivity of the rod system at this point?
What is the relationship between threshold and pigment bleached?
still desensitised by several hundred fold
threshold rises approximately exponentially with the fraction of pigment bleached.
How can bleaching be compared to dark-light
The elevation of threshold after bleaching affects the rod system in much the same way as an increase in the dark-light.
Does bleaching affect individual rods?
yes - directly desensitizes them (bleaching desensitization)
What does bleaching desensitization of individual rods involve
persistent excitation of the phototransduction mechanism by rhodopsin photoproducts, leading to a reduced cytoplasmic [Ca2+] as in light adaptation.
What is post-bleach noise
what can be the effect
Bleaching results in an increased rate of spontaneous quantal events in each rod.
limit the detection within the retina of the responses to dim flashes
Post-bleach noise can limit the detection within the retina of the responses to dim flashes. How?
believed to result from back reactions by quenched forms of photoisomerised rhodopsin, some of which can also weakly excite phototransduction directly.
How is rhodopsin regenerated after bleaching (5)
1) all-trans-retinal
dissociates from opsin,
2) is reduced to all-transretinol and
3) passes from the photoreceptor to
the pigment epithelium in association with
interstitial retinoid binding protein. There, it is
4) reconverted to 11-cis retinal, which
returns to the photoreceptors and 5) reassociates
with opsin to regenerate rhodopsin.
During dark adaptation, there is a progressive change in the passage of photoreceptor signals through the mammalian retina. Describe these changes
What are the cells involved at each stage
photopic range: only the cones function and
the rods are fully saturated. The cone signals pass through the cone circuit via the on and off cone bipolars.
mesopic range: both rods and cones are able to function, and both contribute to ganglion cell responses.
scotopic range:
(the end of dark adaptation)
the rods take over completely, their signals running via the rod bipolar cells to the AII amacrine cells, and finally via the terminals of the cone bipolars to the ganglion cells.
How is the extent of coupling between AII amacrine cells increased during dark adaptation
by the action of the dopaminergic A18 amacrine cells.
How is dopamine involved in retinal amacrine cells
Dopamine (released in the light) decouples gap junctions
between AII amacrine cells.
Thus, in the dark-adapted retina, when dopamine levels are low, the strong coupling between AII amacrine cells allows the rod bipolar signals to reach a larger number of cone
bipolar cells than in the light-adapted retina, thus summing these signals over a larger area.
How does changing illumination change the spatial acuity of the visual system
At low intensities, acuity is low over the entire retina, as the high-convergence rod pathway is used. But as the light intensity increases, foveal acuity improves dramatically as its tightly-packed, densely sampled cones are brought into play
What does high spatial resolution require in the visual system
intensities sufficient to adequately stimulate the cone system.
How can the effect of changing illumination on the temporal properties of vision be assessed
critical fusion frequency:
the frequency above which a flickering light is perceived as steady.
Describe the critical fusion frequency of the visual system at low intensities
At low intensities vision depends on the rods, which
are best stimulated by blue-green light. Rod responses are, however, quite slow, giving
rise to a low flicker fusion frequency which never exceeds 15 Hz
Describe the critical fusion frequency of the visual system at high intensities
At higher intensities the cones take over, and exhibit far better temporal resolution. At high intensities at
which the cone system responds most rapidly, the flicker fusion frequency approaches 60 Hz.
What happens if at low intensities a long wavelength stimulus is used
barely stimulates rods so only the contribution of the cone system is
seen.
True or false
as mean intensity increases, the visual system becomes progressively better at following fast changes.
true as can be seen by assessing critcal fusion frequency (<15Hz in low light, ~60Hz at high intensities)
