Visual cortex and perception Flashcards
What happens at the optic chiasm
Fibres from the nasal portion of both the left and right retina cross over- this means all info from the left visual field is directed to the right side of the brain, and vv
Where is info from each hemifield processed
All info from the left visual hemifield is processed by the right hemisphere, while all info from the right visual hemifield is processed by the left hemisphere
Summarised pathway of visual info through the brain
Retina -> Optic chiasm -> Optic tract -> LGN -> Optic radiation -> V1-> Other subcortical visual nuclei
How is the LGN divided
Split into 6 layers, magnocellular/parvocellular/ koniocellular info goes to different layers
For P and M cells, each layer gets a precise retinotopic input from one eye (ipsi vs contra)
Where does M vs P vs nonMnonP info project to in the LGN
M- layers 1-2
P- layers 3-6
nonMnonP- ventral to each principal layer, called layers K1-6
How are the electrophysiological properties of LGN cells similar to the ganglion cells supplying them
ON and OFF cells remain independent, P cells retain colour opponancy, circular receptive fields with surround antagonism
eg magnocellular LGN neurons have similar properties to M cells
Is there retinotopic mapping in the LGN?
Yes, precise retinotopic map in each layer
Experimental lesion monkey study, effect of damage to magnocelllar layers of LGN
Merrigan et al (1991)- sharp reduction in ability to perceive rapidly changing stimuli, no effect on visual acuity or colour vision
Experimental lesion monkey study, effect of damage to parvocelllar layers of LGN
Merrigan et al (1991)- no effect on motion perception, severely impaired visual acuity and colour perception
Experimental lesion monkey study LGN- conclusion about role of parvocellular stream
Merrigan et al (1991)-Important for high spatial resolution- size, shape and colour of objects
Experimental lesion monkey study LGN- conclusion about role of magnocellular stream
Merrigan et al (1991)-Critical for tasks that require high temporal resolution- location, speed and direction of a rapidly moving object
Why is the striate cortex considered to be the primary visual cortex (V1)
Most LGN axons terminate in V1, all V1 neurons respond exclusively to visual stimuli, ablating V1 causes blindness, electrical stimulation of v1 elicits visual sensations
What is the result of a stroke destroying neurons in the right V1
Loss of left (contralateral) visual field, as V1 is needed for initial cortical processing of visual info necessary for visual perception
Study showing effect of shrapnel wounds on visual field
Holmes- studied different visual field losses caused by different shrapnel wounds causing different V1 lesions in WW1 soldiers.. could map out the whole of the visual field in V1 in these individuals
What is a scotoma
An area of blindness in the visual field- the region of the scotoma is characteristic of the area of the lesion, showing the retinotopic organisation of the visual pathways
What distortion is there in the cortical retinotopic map
Cortical magnification of area receiving and analysing foveal input aka it is disproportionately large
Peripheral areas have much smaller areas for cortical processing
What is the retinotopic map in the cortex based on
No of receptors present in fovea vs periphery, and no of ganglion cells that output that info
What important research did Hubel and Wiesel provide us- development of the visual system?
Critical periods and descriptions of ocular dominance columns
What important research did Hubel and Wiesel provide us- bases for understanding visual physiology
How the brain interprets visual info to generate edge detectors, motion detectors, stereoscopic depth detectors and colour detectors
How is V1 divided
9 layers with distinct cytoarchitecture- I (ventral-most), II, III, IVA/B/Ca/Cbeta, V, VI
Different pathways dock in different layers
What do stellate cells do in v1
Receive info streams from the LGN and pass it to the dendrites of pyrAmidal cells
What carries info from the LGN to V1
Optic radiations
Where does info from the magnocellular pathway terminate in v1
Layer IVCa
Where does info from the parvocellular pathway terminate in V1
Principally IVCbeta
Where does info from the koniocellular pathway terminate in V1
Layers II and III
What do pyramidal cells do in V1
Send info out of V1 to form connections with others areas of the cortex (extrastriate and subcortical areas), allowing horizontal processing by branching within each layer and forming local connections in the cortex
Where is info sent downwards from v1 by pyramidal cells
Some sent to superior colliculus involved in saccadic eye movement, and LGN for intention and arousal to a particular visual scene
What experiment did Hubel and Wiesel carry out into the physiology of V1
Hubel and Wiesel (1950)- systematically did microelectrode recordings of individual neurons in the striate cortex in cats/monkeys to determine their receptive fields, what they responded to etc
What columns did Hubel and Wiesel discover in V1
Info from each eye is segregated in ocular dominance columns in layer IV
What did Hubel and Wiesel discover about neurons in V1 and their receptive field properties
Different neurons showed binocularity, orientation selectivity, direction sensitivity, colour processing
Hubel and Wiesel study evidencing the existence of ocular dominance columns- procedure?
Hubel and Wiesel (1969)- Radioative proline injected into one eye, terminations in V1 visible by putting old fashioned film over it to develop, producing a collection of silver grains- autoradiogram shows terminations as bright bands
Hubel and Wiesel study evidencing the existence of ocular dominance columns- results
Hubel and Wiesel (1969)- Autoradiogram shows white stripes (terminations) are organised into columns
When the experiment was repeated with the other eye, the black and white stripes switched, suggesting they come from the different eyes
What is ocular dominance
The tendency to prefer visual input from one eye over the other
What do electrical recordings confirm about ocular dominance columns
Neurons in layer IV of V1 respond to stimulation of either the left or right eye ie show ocular dominance
What is the retinotopic map in the cortex based on
No of receptors present in fovea vs periphery, and no of ganglion cells that output that info
What important research did Hubel and Wiesel provide us- development of the visual system?
Critical periods and descriptions of ocular dominance columns
What important research did Hubel and Wiesel provide us- bases for understanding visual physiology
How the brain interprets visual info to generate edge detectors, motion detectors, stereoscopic depth detectors and colour detectors
How is V1 divided
9 layers with distinct cytoarchitecture- I (top), II, III, IVA/B/Ca/Cbeta, V, VI
Different pathways dock in different layers
What do stellate cells do in v1
Receive info streams from the LGN and pass it to the dendrites of pyrAmidal cells
What carries info from the LGN to V1
Optic radiations
Where does info from the magnocellular pathway terminate in v1
Layer IVCa
Where does info from the parvocellular pathway terminate in V1
Principally IVCbeta
Where do binocular neurons first appear
Projections from layer IV of V1 to layers above or below show convergence of info from both eyes- most neurons in layers II, III, V and VI are binocular
What do pyramidal cells do in V1
Send info out of V1 to form connections with others areas of the cortex (extrastriate and subcortical areas), allowing horizontal processing
Where is info sent downwards from v1 by pyramidal cells
Some sent to superior colliculus involved in saccadic eye movement, and LGN for intention and arousal to a particular visual scene
What experiment did Hubel and Wiesel carry out into the physiology of V1
Hubel and Wiesel (1950)- systematically did microelectrode recordings of individual neurons in the striate cortex in cats/monkeys to determine their receptive fields, what they responded to etc
What columns did Hubel and Wiesel discover in V1
Info from each eye is segregated in ocular dominance columns in layer IV
What did Hubel and Wiesel discover about neurons in V1 and their receptive field properties
Different neurons showed binocularity, orientation selectivity, direction sensitivity, colour processing
Hubel and Wiesel study evidencing the existence of ocular dominance columns- procedure?
Hubel and Wiesel (1969)- Radioative proline injected into one eye, terminations in V1 visible by putting old fashioned film over it to develop- autoradiogram shows terminations as bright bands
Hubel and Wiesel study evidencing the existence of ocular dominance columns- results
Hubel and Wiesel (1969)- Autoradiogram shows white stripes (terminations) are organised into columns
When the experiment was repeated with the other eye, the black and white stripes switched, suggesting they come from the different eyes
What is ocular dominance
The tendency to prefer visual input from one eye over the other
What do electrical recordings confirm about ocular dominance columns
Neurons in layer IV of V1 respond to stimulation of either the left or right eye ie show ocular dominance
Hubel and Wiesel blindfolded kitten experiment- results in kittens with 1 eye blindfolded to 6 months
Hubel ad Wiesel (1963)- Blind in deprived eye even once blindfold was removed, non-deprived eye assumes control of the whole column
Hubel and Wiesel blindfolded kitten experiment- results in kittens with both eyes blindfolded to 6 months
Hubel ad Wiesel (1963)- vision never improved once blindfold was removed (severely impaired), no ocular dominance columns formed so would never form
Normal LGN connections, normal receptive fields etc
Hubel ad Wiesel (1970)- study blindfolded adult cats results
Had no effect on their vision as ocular dominance columns had already formed
What did Hubel and Wiesel say about the critical window for ocular dominance column development
Lack of environmental stimulation in the critical window severely and irreversibly affects the circuitry in visual cortex, causing an inability to process info from the affected eye
FIRST 3 MONTHS
Study into development of ocular dominance columns with binocular vision vs monocular vision- normal binocular vision
Adams et al (2007)- following normal development of ocular domiance columns, there is an equal no of black and white stripes in immunohistochemistry
What is revealed by inserting a microelectrode perpendicularly down through the various layers of the visual cortex
Reveals neurons of the same orientation preference in a column, regardless of whether they have simple or complex receptive fields
What is revealed by inserting a microelectrode parallel to the surface of the visual cortex
The microelectrode passes through several columns in the same layer revealing a gradual change in orientation preference as the microelectrode progresses
What is retina disparity
Each eye receives a slightly different image when looking at the same point in visual space
Where do binocular neurons first appear
Projections from layer IV of V1 to layers above or below show convergence of info from both eyes
What does binocular fusion form
A single stereoscopic perception of depth and distance
What can result from improper binocular fusion
Double vision- brain may ignore info from weaker eye to prevent this
What is amblyopia
Poor or indistinct vision in an otherwise normal eye- can be caused by strabismus (eye pointing in wrong direction), congenital cataract or refractive errors
What happens in the brain as a result of amblyopia
In children, the brain learns to ignore the vision from the weaker eye and the ocular dominance columns are not properly formed
How can amblyopia be treated
Manipulating V1’s plasticity by forcing stimuli to be received in the poorer eye- patching the good eye, atropine eye drops cause blurring of the good eye, blinding contact lenses in the good eye
When is the critical window for effective amblyopia treatment
Up to 8 years old
How are the compelx cell receptive fields of cells in parvointerblob pathway formed
Stellate cells in layer IV are innervated by parvocellular layers of LGN to form simple cell receptive fields…projections to the interblob layers in layers II and III show complex cell receptive fields
What selectivity do simple cells show
Orientation selectivity- respond to bars of light in a specific orientation (Hubel and Wiesel, 1959)
Describe how simple cells show orientation selectivity
Hubel and Wiesel (1959)- clearly defined ON and OFF regions within the elongated receptive field
Prefer a specific orientation- bars, slits or edges
Which V1 layers are complex cells found in
Layers II, III and V
What do complex cells show selectivity for
Hubel and Wiesel (1959)- Give responses to stimul throughout the receptive field in the correct orientation
How do the receptive fields of complex cells difer from simple cells
Hubel and Wiesel (1959) Complex cells have no distinct excitatory/inhibitory regions, larger more complex receptive fields
How are the receptive fields of simple cells created
Linear receptive fields formed from converging cumulative input from >3 LGN neurons with receptive fields aligned along one axis (so centre ON regions form a line), obvious ON and oFF regions
How are the receptive fields of complex cells created
Composed of several like oriented simple cells, but no obvious ON and OFF regions
What is revealed by inserting a microelectrode perpendicularly down through the various layers of the visual cortex
Reveals neurons of the same orientation preference in a column, regardless of whether they have simple or complex receptive fields
How did Hubel and Wiesel describe orientation columns in V1
The cortex is organised into adjacent columsn with an orientation preference that differs by 15degrees
All 180degrees is represented every 1mm of cortex- represents all orientations for a particular area of visual space
What are the blobs in V1
Layers II and III are segregated into blobs surrounded by interblobs, with each blob centred on an ocular dominance column- response properties of neurons in the blobs are different
Evidence for the blob and interblob regions
Carrol and Wong-Riley (1984)- immunohistochemical labelling for cytochrome oxidase (enzyme for cell metabolism) reveals cytochrome-rich BLOBS surrounded by interblob regions
What does horizontal processing in the LGN lead to the formatino of
A full visual perception of the visual field
What do blobs receive info from
Direct LGN input from single opponent koniocellular layers, parvocellular and magnocellular input from layer IVC of the striate
What do the interblob regions receive info from
Parvocellular input from layer IVC
Why do people criticse the hypercolumn nodel
It does not allow for obvious inclusion of other properties such as colour, optical images of V1 activity show the regions of V1 responding to different eyes and orientations are not nearly as regular as the hypercolumn model
What is the parvointerblob pathway responsible for
Discriminative ‘form or shape’ processing cells of V1
How are the compelx cell receptive fields of cells in parvointerblob pathway formed
Stellate cells in layer IV are innervated by parvocellular layers of LGN to form simple cell receptive fields…projections to the interblob layers in layers II and III show complex cell receptive fields
What are the properties of interblob neurons
Orientation-selective necessary for fine detail processing, wavelength insensitive, respond to achromatic contrast, binocular
What sort of cells are the cells in the blobs in V1
Concentric double-opponent cells
What are the concentric double-opponent cells in the blobs in V1
Respond selectively to colour contrast eg excited by green and inhibited by red in its receptive field centre, and excited by red and inhibited by green in its receptive field surround
Don’t respond well to uniform illumination or achromatic contrast
What are the 4 classes of double opponent cels in the blob pathway
G+R- centre/G-R+ surroudn and vv
B+Y-centre/B-Y+surround and vv
What are the properties of neurons in the blob areas
Wavelength sensitive, detect colour contrast via double colour opponent receptive fields, insensitive to achromatic contrast, monocular, orientation/direction INSENSITIVE
What are double opponent cells formed from
Opponent cells
What are the 3 pathways that follow the Parvocellular magnocelular and koniocellular pathways
Blob pathway, parvointerblob pathway, magnocellular pathway
What does direction sensitivity mean
With a moving bar stimulus presented at the optimal orientation, the neuron responds strongly when the bar is swept to the right, but weakly when the bar is swept to the left
What is the magnocellular pathway involved in
Analysis of moving stimuli, control of visual attention and gaze, stereopsis (depth perception)
What innervates the magnocellular pathway
Layer IVCa receives input from M layers of LGN forming simple cell receptive fields, projects to layer IVB which is made up of simple and complex cells
Akinetopsia case study- how was the patient’s visuomotor coordination impaired
Zihl (1983)- Asked to move her finger along a wire as fast as possible- performance was much poorer in visual than tactile conditions, as the woman reported she could not follow her finger with her eyes if she moved too fast
How is info from the M pathway output to control visual attention and gaze reflexes
Via layer V outputs to the pulvinar (thalamic nucleus involved in visual attention), superior colliculus (saccadic eye movements) and pons
What model do Hubel and Wiesel propose to explain how the visual scene is broken down and processed
Hypercolumn model- hypercolumns are functional modules
How did Hubel and Wiesel demonstrate the hypercolumn model experimentally
Using microelectrodes to explore the receptive fields of the neurons in V1, they showed it can be divided into essentially identical columns
The columns differ in the portion of the visual field assigned to them
What does achromatopsia suggest about visual processing
Results from damage to temporal and occipital lobes, with normal LGN and V1- suggests disorder of processing in ventral stream
What does each column in Hubel and Wiesel’s hypercolumn model contain
Cells of every direction orientation selectivity possible, right and left eye, info from different layers etc
Where does visual processing occur beyond V1
In over 30 retinotopically mapped areas
Where do layers II III and IVB of V1 provide output to
Project to other cortical layers
Where does layer VI OF V1 provide output to
Projects back to LGN
What 2 parallel streams is info processed in after V1
Dorsal stream and ventral stream
What is the dorsal stream fed by
Magnocellular neurons in V1
What is the dorsal stream involved with
WHERE PATHWAY- motion recognition, visual motion, control of actions
What is the ventral stream fed by
Parvointerblob and blob neurons in V1
What is the ventral stream involved with
WHAT PATHWAY- object/form recognition, perception of the visual world
What is area V5 also known as
MT- medial temporal
What is V5 involved in
Detection of motion
What is the result of bilateral damage to V5
Akinetopsia, inability to perceive visual motion
Akinetopsia case study- how was the patient’s visuomotor coordination impaired
Asked to move her finger along a wire as fast as possible- performance was much poorer in visual than tactile conditions, as the woman reported she could not follow her finger with her eyes if she moved too fast
What is area V4 involved in
Shape and colour recognition
What does electrophysiology suggest about selectivity of V4 neurons
V4 neurons are both orientation and colour selective
What is achromatopsia
Loss of colour vision despite normal functioning cones, also associated with deficits in form perception
What does achromatopsia suggest about visual processing
Results from damage to temporal and occipital lobes, but normal LGN and V1- suggests disorder of processing in ventral stream
What lobes do the dorsal and ventral streams project to
Ventral stream- temporal lobe
Dorsal stream- parietal lobe
Case study into blindsight- what was the case
Weiskrantz(1986)- Man had blindsight after complete bilateral loss of V1- registered as blind by all physiological tests, imagingi studied showed inactive V1
Case study into blindsight- what were the findings
Weiskrantz (1986)- man was able to walk down a cluttered hallway avoiding objects
He has a pathway where info from LGN and thalamus is used to achieve this, without it passing through V1 meaning he can’t perceive it
How do the ganglion cells first leave the eye
Optic nerves exit the optic disks and travel thruogh the fatty tissue behind the eyes
Why is the crossing over in the optic chiasm called partial decussation
Only the axons from the nasal retinas decussate
What are the receptive fields of cells in the koniocellular LGN layers like
Centre-surround, light/dark or colour opponency
How much of the LGN’s input comes from V1
80% of excitatory synapses
What is a possible role for projections from V1 to LGN
‘Top-down’modulation from V1 to LGN gates ‘bottom-up’ input back to cortex eg suppressing inputs coming from outside an area in our visual field we wish to fixate i
Where does the LGN receive input from other than the retina and V1
Brain stem neurons involved in alterness and attentiveness- input can modulate the magnitude ot LGN responses to visual stimuli
What are other names for V1
Brodmann’s area 17, striate cortex
In which lobe is V1 located
Occipital lobe
How is there retinotopy in the projections from retina to LGN and V1
Neighbouring retinal cells feed info to neighbouring places in LGN and V1, so 2D surface of retina is mapped onto the 2D surface of the subsequent structures
What are the 2 types of neurons in V1
Spiny stellate cells and pyramidal cells
Where are stellate cells found in v1
Found in the 2 tiers of layer IVC
Where are pyramidal cells found in V1
Outside layer IVC
What is the structrue of stellate cells
Small with spine-covered dendrites that radiate from the cell body
What is the structure of pyramidal cells
Covered in spines also, single thing apical dendrite that branches as it ascends towards layer, and multiple basal dendrites that extend horizontally
In which V1 layer do most axons from the LGN terminate
IVC
Why does layer IVC contain 2 overlapping retinotopic maps
One from the magnocellular LGN, one from the parvocellular LGN
What is the consequence of most V1 intracortical connections extending perpendicular to the cortical surface along radial lines
Maintains the retinotopic organisation in layer IV, meaning a cell in layer VI receives info from the same part of the retina as the cell perpendicular to it in layer IV
Where does info from the left and right eye mix for the first time
Layers IVB and III, where they are innervated by stellate cells projecting from layer IVC
What do recent studies suggest about the blob/interblob theory
Recent V1 studies have found overall neurons in blobs and interblobs are similar, with both showing orientation and colour selectivity- no simple way to distinguish the receptive field properties of blob cells from interblob cells
How is the reality of the blob/parvointerblob/magnocellular pathways mroe complicated
The 3 pathways don’t keep m/p/nonMnonP signals separate as they mix, striate cortex output has a different form of parallel processing (ventral vs dorsal streams)
What did Hubel and Wiesel argue would be the result of removal of one hypercolumn
Would leave a blind spot in the visual field, as each of the 1000s of hypercolumns analyse a small point of light from the image
Which of the previous 3 pathways are the dorsal and ventral stream pathways similae to
Dorsal stream- magnocellular
Ventral stream- blob, parvointerblob
How does visual info progress as it leaves V1
Projects to V2, V3, ….progression of areas where more complex specialised visual representations develop
What are the receptive fields of neurons in MT
Large receptive fields that respond to stimulus movement in a narrow range of directions- almost all cells are direction selective
Evidence for role of MT in movement
MT has been shown to be activated by some optical illusions that produce illusory motion, suggesting its neurons tell us perceived motion rather than actual present motion
How is MT organised similar to V1
Arranged into direction-of-motion columns- perception of motion presumably depends on a comparison of the activity across columns spanning a full 360 degrees of preferred directions
Study showing role of MT in monkeys
Newsome- weak electrical stimulation in MT in monkeys appears to alter the direction small dots of light are perceived to move - monkey behaviourally reports a perceived direction of motion based on COMBINATION of MT stimulation and visual motion input
What is area MST
Area beyond MT, medial superior temporal, contains cells sensitive for linear motion, radial motion and circular motion
What appears to be the farthest extent of visual processing in the ventral stream
An area in the inferior temporal lobe called area IT
What is the fusiform face area
Kanwisher et al (1995) found the fusiform face area, an area on the fusiform gyrus especially sensitive to faces- propopagnosia associated with damage to an area that may include the fusiform face area
Evidence against idea of ‘grandmother cells’
No evidence for this region, coutner to broad tuning, too risky
Evidence against idea of ‘grandmother cells’- no evidence for this region
No evidence a portion of the cortex has different cells tuned to each of the millions of objects we all reconise
Evidence against idea of ‘grandmother cells’- counter to broad tuning
Such great selectivity is counter to the general principle of broad tuning that exists throughout the nervous system- photoreceptors respond to a range of wavelengths, simple cells to many orientations
Evidence against idea of ‘grandmother cells’- too risky?
Too risky for the nervous system to rely on extreme sensitivity- a blwo to the head might kill all 5 grandmother cells, meaning we instantly lose the ability to recognise her
How many LGNs are there
2, one in each hemisphere
How much of the LGN represent the fovea and the region just around it
Half the neural mass of LGN
How do the local interconections of cels in the V1 columns allow a new level of abstracion
Each column contains many complex cells that receive direct connections from the simple cells in the column
