Colour perception Flashcards
why colour vision
- enriches perceptual experiences
- another dimension for object boundary discrimination (detecting chromatic contrasts between adjoining objects) & object identification/recognition
- survival value
what is the primary visual pathway interested in
wavelength discrimination i.e. the nature of the chromatic sensitivity of the primary area v1 neurons, areas include:
- cones
- RGCs & the LGN
- primary v1 cortex
what do cones have which makes them wavelength selective
pigments within their outer segments which selectively respond to, short, middle or long wavelength selectivity
what do RGCs & the LGN have which makes them wavelength selective
- red/green & blue/yellow wavelength opponency, involved with wavelength discrimination
what does the primary v1 cortex have which makes them wavelength selective
- red/green & blue/yellow + mixed (red/green & blue/yellow) and double wavelength opponency
what is the extra striate area (v4) cortex and beyond interested in
colours:
- colour perception & constancy (damage to v4 = achromatopsia)
- colour discrimination & knowledge
what was the first area responsible for colour vision
area V4 in the lingual gyrus
what did sir isaac newtons optiks (1704) experiment show
that light is composed of different wavelengths of light, perceived by us as different colours, from 400nm (blue) to 700nm (red)
which part of newton’s (1704) statement is correct about our colour vision
‘every surface reflects the rays of its own colour more copiously than the rest’
which means colour vision indicates we have colour detectors in our eyes which makes us able to discriminate between different wavelengths or perceive colours that way
which theory does Thomas young (1773-1829) have about colour vision
trichromatic theory:
the human visual system can discriminate between wavelengths differing by only 1-2nm over the total 300nm of the visible spectrum i.e. we can detect ~200 different hues, and because of this, ‘it is impossible to conceive that each sensitive point on the retina contains an infinite number of (receptors), capable of detecting every visible hue, it is necessary to suppose their number is limited to the 3 primary colours, red, green & blue.’
so the number of receptors that we have on our retina is limited and theres no space for 200 hues and at every single location on the retinal surface
what are the colours that cannot be created by mixing other colours together
blue, green & red: the primary colours unlike: yellow = green + red turquoise = green + blue purple = blue + red
what is young’s trichromacy theory supported by
the existence of 3 cone types in the human retina containing variance of the visual pigment rhodopsin, with different spectral sensitivities
what is the peak absorption and range of S cones
peak: 420nm (blue)
range: 400-530nm
what is the peak absorption and range of M cones
peak: 533nm (green)
range: 450-630nm
what is the peak absorption and range of L cones
peak: 564nm (redish)
range: 480-700nm
what are the two techniques for showing that the chromatic sensitivities & ‘tuning curves’ of the 3 isolated cone types showing similar absorption profiles & action spectra
- micro spectro photometry: absorption profile
- intra-cellular electrophysiological recordings - action spectra
how is an action spectra taken by intra-cellular electrophysiological recordings taken, for showing the chromatic sensitivities & ‘tuning curves’ of the 3 isolated cone types
by putting a micro electrode into the outer segment of an individual cone & shining different wavelengths of light upon its outer segment & looking at the change of membrane potential
what did both techniques of micro spectra photometry and intra-cellular electrophysiology reveal
eg an M cone has a peak absorption of 533nm but, it also absorbs blue & red colours (at a lower sensitivity) so theres a wide range of selectivity. this is same for S blue cones and L red long cones.
how many types of cone pigment are required for colour vision
at least 2, or more to increase discrimination
why is one cone pigment not enough to require colour vision
one cone pigment cannot discriminate colours of the same intensity, as equal relative absorptions/neural responses occur at different wavelengths (e.g. 430nm blue & 550nm green)
so leads to exact same level of absorption by this photoreceptor, so cannot tell difference between blue & green with one cone pigment as it leads to the same response and thats why colour vision at night is poor as rods are in use and rods cannot discriminate different wavelengths
why are 2 cone pigments required for colour vision
the combined outputs of 2 cones can differentiate these wavelengths as ‘blue’ (430) is A:45% & B:20% (= unique) & ‘green’ (550) is A:45% & B:100% (= also unique)
describe Ewald Hering (1834-1918) opponent theory
because 4 colours (red, green, blue, yellow) are never seen merging together at the same point in space (e.g. no word for ‘reddish-green’ or ‘blueish-yellow’ Hering proposed that they are combined at higher levels of the visual system in a ‘mutually destructive’ i.e. opponent manner
red vs green opponency
blue vs yellow opponency
what is Hering’s theory supported by
psychophysics: adaptation results in perception of the opponent colours
&
physiological recordings showing 2 types of chromatically opponent RGC’s in the retina
what are the two types of physiological recordings showing 2 types of chromatically opponent RGC’s in the retina
type 1: with red-green opponent, centre-surround RFs
type 2: red-green or blue-yellow spatially overlapping opponent RFs
describe type 1: with red-green opponent, centre-surround RFs of physiological recordings of chromatically opponent RGC’s in the retina
- one cone type (L or M) mediates the RF centre
- the antagonistic cone type (M or L) mediates the RF surround
describe type 2: red-green or blue-yelow spatially overlapping RFs of physiological recordings of chromatically opponent RGC’s in the retina
- red/green: one cone type (L or M) mediates the ON response, the antagonistic cone type (M or L) mediates the OFF response
- blue/yellow: S cone type mediates the ON response, combined inputs from both the L & M yellow cones mediate the overlapping OFF response placed anywhere in its RF
which type of physiological recordings of chromatically opponent RGC’s in the retina does not have a centre surround component
type 2, instead they have short wavelength cones which mediates the ON response anywhere in its RF, combined with inputs from both L & M cones
so they’re colour opponent but don’t have spatial component in their RFs
by how much does each type of cone input & RGC RFs account for
- centre-surround opponent - 75% (antagonistic)
- overlapping opponent - 10%
- centre-surround achromatic brightness - 15%
what is the achromatic centre-surround RF mediated by
parasol/magno = saturation/brightness of cell (luminance contrast)
in type 1 red-green opponent RGC, when does the RF respond maximally
L-wave ON stimulation of its RF centre when there is very little or no M-wave light (OFF) in its surround i.e. no green in its antagonistic surround
in type 1 red-green opponent RGC, when does the RF respond less well
to diffuse L-wave light, as red cones are slightly responsive, so its inhibiting the cell response
in type 1 red-green opponent RGC, when does the RF respond minimally
when it is inhibited by simultaneous (mutually destructive) L-wave & M-wave ON-stimulation in both its centre & antagonistic surround because the excitatory L and inhibitory M cone inputs cancel each other out
so RGC reports nothing to the brain
in type 2 blue-yellow opponent RGC, when does the RF respond maximally
S wave blue ON-stimulation or to L+M wave yellow OFF-stimulation anywhere in its RF (i.e. same response as yellow light being switched off anywhere in its RF, so doesn’t give a response to yellow light being on, but a big response to yellow light being turned off)
in type 2 blue-yellow opponent RGC, when does the RF respond minimally
when blue & yellow are ON together anywhere in its RF, the excitatory blue ON & inhibitory yellow ON responses cancel out by mutual destruction/opponency (antagonistic)
how much do type 1 RGCs with red ON centre and green OFF surround account for
majority 90% of neurons
how much do type 2 RGCs with blue-allow opponent RGCs account for
minority out of the 10% of type 2 neurons only 5% are blue ON & yellow OFF
thats why people with glaucoma report that the first thing they complain of which is to do with colour vision is blue-yellow discrimination as its only 5% so will easily get lost
what does the parallel chromatic-opponent pathways system does type 1 red/green opponency belong to
the parvo system:
- midget RGCs & LGN parvo cells send axons to..
- area v1 makes connections with granule cells in layer 4Cbeta & some CO blob cells which are above and below 4Cbeta
what does the parallel chromatic-opponent pathways system does type 2 blue/yellow opponency belong to
the konio system:
- small bistratified RGCs & LGN konio cells send axons to…
- area v1 which bypass layer 4C & go straight to other CO blobs cells to layers above and below 4C
what does the parallel chromatic-opponent pathways system does area v1 belong to
wavelength-selective ‘blob’ cells:
- circular RFs with opponent properties, similar to those of type 1 & 2 RGCs & LGN neurons (i.e. majority of blob cells have red/green & blue/yellow opponency)
what are the several important changes to the way in which chromatic information is processed in v1
- amplification of the blue-yellow channel (x5)
- cross-channel mixing
- within-channel mixing
how is amplification of blue-yellow channel x5 an important change to the way in which chromatic information is processed in v1
whereas only ~5% of RGCs are blue-yellow selective, ~25% of CO blobs contain exclusively blue-yellow opponent processing cells
i.e. theres a big increase in v1 in emphasis to blue-yellow component processing, compared to the retina
how is cross-channel mixing an important change to the way in which chromatic information is processed in v1
recent evidence shows that many CO blobs have ‘bridges’ (passing through the inter blob zone) containing cells with mixed R-G & B-Y RFs, representing convergent inputs from the 2 chromatic channels
ie red-green opponency becomes combined with blue-yellow opponency = a completely new type of opponency. cells within the bridges is where the cross channels occurs
how is within-channel mixing an important change to the way in which chromatic information is processed in v1
- a significant proportion of cells in the R-G blobs or bridges show another new property known as ‘double wavelength opponency’ due to convergent within-channel (R-G & G-R) inputs of opposite sign
- which makes them maximally responsive to these chromatic contrasts, rather than being inhibited by them (as in the retina & LGN)
describe in vivo optical imaging method
wide field stimuli:
- different orientations of chromatic contrasts presented to one eye
camera images a path of v1 cortex for oxygen utilisation (related to neural activity that the cell is engaged in)
- neural activity (dark=CO blobs, colour; pale=interblobs (non-responsive cells to chromatic stimuli), achromatic=interested in orientation
what are optically imaged blobs & bridges
some blobs are joined by bridges with the mixed or double wavelength opponency (which look like dumbbells instead of blobs)
what do the optically imaged blobs & bridges contain
chromatic sensitivity neurons in CO blobs
what are majority of colour responses confined to, (instead of optically imaged blobs & bridges)
to isolated blobs:
- ~75% interested in R-G colour opponency
- ~25% interested in B-Y colour opponency
what is cross channel mixing
turquoise-orange opponent RF: v1 cell in a CO ‘bridge’ region:
- ON centre
maximal response at 480nm (turquoise)
weaker response to blue (450nm) & to green (530nm)
- OFF surround
maximal response at 600nm (orange)
weaker response to yellow (570nm) & to red (630nm)
turquoise-orange opponent Rf = B-Y + R-G opponency
YOU DO NOT SEE THIS RF COMBO IN THE RETINA OR LGN
what is, within-channel mixing
double-wavelength opponent v1 cell in a CO bridge region: chromatic contrast discrimination
there is a red ON centre, OFF surround
and a green ON surround, OFF centre
so a cell prefers red ON centre & green ON surround
which gives off a response or is inhibited by red in its surround & green in its surround
e.g. if you shine red in its centre, where theres very little green = cell likes it & if you shine green in its surround with very little red = cell also likes it
which is excited by real chromatic contrast in the real world
which cells only respond to wavelengths of light reflected from a surface and not the colours of surfaces in the scene
chromatically-sensitive cells at low light levels of the visual system: retina, LGN, v1 & v2
how is the perceived colour of a surface in relation to the spectral composition of the illuminating light of the surface and what is this known as
it is normally relatively independent of the spectral composition of the illuminating light of the surface
eg in A130 lecture theatre, most of the most incident light is short wave blue, so all the surfaces will naturally reflect more short wave than middle or long wave light, yet red surfaces (chairs) are still perceived as red, irrespective of illumination thats falling upon them
KNOWN AS COLOUR CONSTANCY
what must colour constancy be mediated by
higher levels of the visual system than v1 & v2
which part of Hering’s statement of colour constancy is true
‘surfaces known from experience are seen through the spectacles of colour memory’ e.g. we know an orange is orange because we know it from memory
what is colour constancy a property of
relatively early sensory processing in cortical area v4 in the lingual gyri
what happened in Zeki’s experiment and what was the outcome on the results
- recorded cells in v1 & v4 and first determined their responses to different wavelengths (action spectra)
- then used multi-coloured (Mondrian) displays illuminated by three projectors shining different amounts of S, M & L wave light into the display & measured the amounts of reflected S, M & L (with a photometer) from specific coloured regions placed in the cells RF (so different regions of the display will reflect back into the monkeys eyes and into its visual system & could control different amounts of wavelengths illuminating the display)
in Zeki’s experiment, what did responses of v1 cells reveal
they depended only on the reflected wavelength composition (the amount of S, M & L wavelengths reflected from the surface, regardless of what colour it was)
in Zeki’s expaeiment, what did responses of v4 cells reveal
v4 cells were colour constant e.g. red cells in v4 only responded to surfaces perceived by humans as being red & not to surfaces perceived as being green or blue even when they reflected much more long wave than middle or short wave light
what was the appearance of the Mondrian when illuminated with red light
illuminated by and reflected much more L than M or S wave light, red areas still looked red, but blue hues look more purple/violet as red mixed with blue make purple
which cells are wavelength dependent and have no correlation with colour perception
v1
explain how v1 cells are only wavelength dependent and have no correlation with colour perception which was carried out in zeki’s experiment
in the red illuminated display, the v1 cell is long wave selective and it responds equally well to any region of the Mondrian display placed in its RF, when that region reflects more LW than MW or SW light
therefore this cell doesn’t exhibit colour constancy
it cannot discriminate between these different colours, only interested in the amount of long wave light reflected from picture into eye
which cells are wavelength dependent and correlated with colour perception
v4 cells
explain how v4 cells are wavelength dependent and correlated with colour perception which was carried out in zeki’s experiment
in the red illuminated display, the v4 cell is long wave selective but it only responds to regions of the Mondrian that look red to human observers & not to other regions reflecting LW light in its RF
no responses at all from blue, green & yellow
explain how area v4 cells are wavelength dependent and correlated with colour perception
eg
if a green surface reflects incidence light in the ratio S:5 M:10 L:5
different from a neighbouring red surface with ratio S:1 M:1 L:10
so if the incident light is mainly ‘red’ with a ratio of S:1 M:1 L:10, then a green surface will reflect back S:5 M:10 L:50, whereas a red surface will reflect back S:1 M:1 L:100
it is by computing these relative reflectance ratios from the surface within their RFs & comparing it to those of other nearby surfaces, that allows a red v4 cell for example to determine whether there is a red surface in its RF rather than a green one
the distinction between red surface to the green surface is the red surface still reflects back alot more long wavelength light than a green surface does = how you make discrimination between surfaces & that mediates colour constancy, but in order to do this, you need things to compare the e.g. red surface with in the FOV = what v4 cells do which need to compare red with another surface to know that the red likes to reflect back a lot of long wave light
what can other surfaces needed for comparison in order to make discriminations between surfaces that makes colour constancy in area v4, also influence
the precise hue perceived i.e. the surround can influence the perceived hue of the centre so colour constancy is not perfect but still important to identify objects
explain the significance for human colour perception = functional specialisations
the lingual gyrus of inferior occipital cortex in each hemisphere contains area v4 specialised for colour perception & colour constancy in the opposite hemi-field:
- functional brain imaging studies in healthy subjects, comparing cortical activations when viewing coloured vs achromatic (grayscale versions) of the same stimuli
- neurological lesions affecting the lingual gyrus which results in selective deficits in colour perception = achromatopsia or dyschromatopsia in milder cases, characterised by loss of colour constancy mechanisms
which stream is area v4 located in the lingual gyrus apart of
ventral stream
name the two types of colour ‘blindness’
- congenital/inherited dichromacy
2. acquired cerebral achromatopsia
describe what occurs in congenital/inherited dichromacy
- only 2 types of cones with functioning pigments (i.e. only two cones are working)
- absence, deficiency &/or confusion in perceiving ONE of the primary colours
what does a person with deuteranopia report
no or murky green: confuse orange with brown
as they lack the middle wavelength component
what does a person with tritanopia report
no blue: confuse blue with green & yellow with violet
as they lack the short wavelength component
what does a person with protanopia report
no red: confuse deep red with black or dark green (can still see yellow)
as they lack the long wavelength component
name some simple colour vision tests
- ishihara plates
- farnsworth-munsell 100 hue
describe what occurs in acquired cerebral achromatopsia
lingual gyrus damage = no colours at all, just greyscale
e.g. left semi-achromatopsia: patient with a local lesion in area v4 of the right lingual gyrus & he can’t see colour in the left hemifield
his attempt to reproduce the colours of a Mondrian in his left hemi-field: sees the shapes, but colours are incorrect & based on wavelength discrimination by via his intact areas v1/v2
what is usually intact in a typical achromatopsia case
visual fields
VA
SA
motion perception
what do patients with typical achromatopsia report, and what sort of tests do they fail on
report the world as appearing in shades of grey
- fail farnsworth munsell 100 hue test (colour sorting)
- can’t find the odd colour out even when its the only colour amongst various shades of grey
what do patients with typical achromatopsia have absence of, but can still detect
- absence of colour constancy
- but can detect chromatic borders between adjoining surfaces, based on intact wavelength discrimination in v1/v2 without being able to see actual colours
what other usual defects do patients with typical achromatopsia have due to non local ventral cortex damage
- upper quadrantanopia (damage to lower bank of calcarine sulcus)
- form agnosia & prosopagnosia (damage to LOC & fusiform face area)
when is area v4 selectively activated
when normal subjects passively view coloured vs greyscale stimuli
when does another area also becomes active when area v4 is selectively active when passively viewing coloured vs greyscale stimuli
the posterior fusiform gyrus when subjects:
- engage in more active colour discrimination tasks
- or view scenes containing un-natural colours (i.e. when making judgements based on prior knowledge of familiar object colours/’through the spectacles of colour memory’)
state when an increased v4 activity + posterior FG is active more anteriorly
when actively discriminating hues in chromatic vs achromatic stimuli
OR
when viewing blue strawberries i.e. a picture of wrong colours which reveals that it does not belong to our colour memory
state when only area v4 is activated
passive viewing of chromatic vs achromatic stimuli
