Exam 4: Visual system Flashcards
what is the retinal microcircuit?
photoreceptors => bipolar cell => retinal ganglion
which retinal cell responds to light?
photoreceptors
fovea
used for fined vision ⇒ 15 degrees off there is the optic disk
optic disk
the collection of the retinal ganglion cells that exit at one point
T/F there are photoreceptors at the exit point of the retina?
False there are none
what are all the layers of the retina? (8)
(distal side)
- pigment epithelium
- photoreceptor outer segments
- outer nuclear layer
- outer plexiform layer
- inner nuclear layer
- inner plexiform layer
- ganglion cell layer
- nerve fiber layer
(proximal side)
which retinal layers are bipolar cells in?
from the outer plexiform to the inner nuclear and inner plexiform layers
what are the size dimensions of photoreceptors?
50 micrometers long and 2-4 micrometers wide
T/f the larger the intensity of the light stimulus the stronger the hyperpolarization?
true
what is the resting membrane potential like for photoreceptor cells?
relatively depolarized but not positive in comparison to other cells
T/F retinal photoreceptors do not fire action potentials?
True
Rods
twilight/dim vision, sustained response ⇒ hundreds of ms long to a brief light visual stimulus
- They are also starving for photons ⇒ we can perceive a single photon if we are in an empty dark room
- If you have pooling across multiple polar receptors then the bipolar cell is excited enough to release signals and stimulate the pathway
when are rods saturated?
in daylight because they are sensitive
what is the acuity of rods?
there is no spatial acuity because of the pooling ⇒ many of them converge on one bipolar rod cell
Cones
daylight vision, transient response ⇒ <100 ms duration to a brief light visual stimulus
what is the acuity of cones?
High acuity with 1 cone to 1 cone bipolar cell
what is the role of cGMP in photoreceptors?
they allow for Na+ channels to be open in the dark which creates the depolarization
dark current
there is an ion channel open in the dark because there is lots of cGMP floating around in the outer segment
what happens to cGMP when light hits the photoreceptor?
cGMP channels are closed and cGMP is reduced ⇒ it gets hydrolyzed and it cannot bind to the channel anymore
- This allows the receptor to hyperpolarize to light
- Potassium is still going outside the cell
how does the photopigment change when light hits the photoreceptor?
rhodopsin changes from 11-cis retinal to all trans retinal
- changes the opsin which activates other molecules
Phosphodiesterase (PDE)
hydrolyzes cGMP
how does signal amplification work in the photoreceptor when light hits? (pathway)
the light activates rhodopsin to activate transducin
- the G protein on transducer breaks off which activates phosphodiesterase (PDE)
- this hydrolyzes the cGMP
- the cGMP channels close and Na+ can no longer get in through them
- one photon closes about 200 ion channels
how fast is the visual system compared to other systems like mechanoreceptors?
Mechanoreceptors respond in 1-2 ms so vision is relatively slow in comparison to some of the other sensory systems
which photoreceptor membrane is rhodopsin located in?
the dark membrane
- the inside of this is called the disk
- the outer membrane has the ion channels
where are the most rods and cones in the retina?
- there are relatively more rods than cones when it comes to density outside of the fovea
- cone density is highest at fovea
- Fovea is 0 eccentricity and the optic disk is 15 degrees off without photoreceptors
which wavelengths do the photoreceptors respond to?
- blue: (short) 400-490 nm
- green: (medium) 450-610 nm
- red: (long) 470-650 nm
what nm wavelength do rods respond to?
about 420-580 nm
T/F retinal ganglion cells compare the activity of at least 2 different cone classes?
True
- The cones can respond to multiple different bands such as overlap between red to green
What is different about primates photoreceptors compared to other mammals? What’s it called to have our photoreceptors?
only primates have all 3 photoreceptors
- Colorblindness rarely means that a human is missing all 3 cones
- called a normal trichromat
Protanopia
color blindness where the red cones are missing
Visual field
the area of space or the external world that can be seen when the eyes are fixated on one point and the head does not move
- A single neuron sees a small part of the visual world
Point of fixation
the point in visual space that fall on the fovea
receptive field (vision)
specific properties of a stimulus that evokes the strongest response from a neuron
- A region of the retina must be illuminated in order to get a response in any given fiber
when will on-center ganglion cells respond?
when there is light in the center and dark in the surround
when will off-center ganglion cells respond?
when there is dark in the center relative to the surround
which cells in the retina are the only ones that fire action potentials?
retinal ganglion cells
what happens when the entire on center and off center is illuminated? what about when it is all dark?
minimal spontaneous firing of action potentials for both on center and off ganglion cells; no firing aside from spontaneous firing
- the pathways work in a complementary fashion to one another
how do we know surround is antagonistic?
activation of the center and the surround simultaneously mostly cancels the response as if there was no stimulus to begin with
what happens if you lose the on-center pathway?
you lose the ability to detect stimuli that are brighter than background
- You can still see objects that are darker than the background
- No useful information in diffuse light
what is the job of the retina?
contrast
- The visual system doesn’t care about uniform luminance
how does the off-center pathway work with stimulation from light?
- The photoreceptor hyperpolarized so there is less release of glutamate (it is normally released)
- The bipolar cell hyperpolarizes from lack of signaling to AMPA/Kinate receptors (releases less glutamate)
- The retinal ganglion cell is hyperpolarized and fires less action potentials to the light stimulus in the off center retinal ganglion cell (releases less glutamate)
- no signal goes to the thalamus
How does the on-pathway pathway work with stimulation from light?
- the photoreceptor cell releases less glutamate to bind to mGluR’s (releases G protein inside)
- the G protein closes TRPM1 channels but with light they stay open so the on-center cell becomes depolarized and releases glutamate
- the ganglion cell becomes depolarized and sends signals to the thalamus
how does glutamate connect to the mGlu channels and the TRPM1 channel?
when glutamate is released in the absence of light it binds to the mGlu channel and activates its G protein to close TRPM1
- when the photoreceptor is excited it releases less glutamate so the TRPM1 ends up staying open
TRPM1
cation channel which causes hyperpolarization of the ON bipolar cell when closed via glutamate
what is the molecular pathway when light is shone in an on-center spot?
the bipolar cell hyper polarizes and the off center pathway will stop firing from a lack of glutamate
- the on center bipolar cell will depolarize from lack of glutamate so TRPM1 will turn on and depolarize the on center ganglion cell to fire action potentials
- cGMP will also be hydrolyzed
what happens when you decrease luminance?
the photoreceptor depolarizes
what is the molecular pathway when a dark spot is on an on-center spot?
- the darkness opens cGMP channels as more cGMP goes to the outside of the photoreceptors which will release glutamate
- the on center bipolar cell will have glutamate that stimulates the mGlu receptors so that they will shut TRPM1 (hyperpolarizing the cell) and this will hyper polarize the retinal ganglion cell to not fire
- the off center ganglion cell will have its AMPA/Kinate channels opened which lets Na+ into the cell to depolarize it and this will release glutamate to depolarize the ganglion cell (fires action potentials)
what is the receptive field surround mediated by?
horizontal cells in the retina that release GABA
Herman grid
center surround mutual antagonism of RGCs responses
- ON center cell at the corner of all 4 squares will have smaller response because center is light and less of surround is dark → center looks kind of gray
- ON center cell between the edges of two squares will have greater response because center is light and surround is more dark (optimal drive of the two cells)
how is the visual field altered by the retina? Fovea placement?
they are inverted and reflected
- the top right of the visual field gets flipped to the bottom left in the retina for both eyes
- the fovea is in the center of the quadrants but skewed toward the nasal side which projects it more lateral in the retinal reflection
Where in the cortex does something in your far left (A) visual field project; middle left (B); middle right (C); far right (D)
- A would project to the right retinal region of the left eye but not reach the right eye and this will cross over at the optic chiasm to go to the right visual cortex
- B would appear in the left and right eyes on the right retinal regions but cross over on the left eye (nasal side) and go straight back on the right eye (temporal side)
- C would appear in the left and right eyes on the left retinal regions but cross over on the right eye (nasal side) and go straight back on the left eye (temporal side)
- D would project to the left retinal region of the right eye but not reach the left eye and this will cross over at the optic chiasm to go to the left visual cortex
Note: for A and D they will not reach the opposite eye because they are too far out of view, but B and C will project to both the left and right eye
is there more white or gray matter in the brain?
more white matter
- if the organization was random we would need a lot more wiring for the neurons to talk to one another
retinotopy
adjacent neurons are encoding similar parts of the visual world to optimize wiring
scotoma
black holes in your visual world ⇒ after damage at different points along the primary visual pathway
- Lesions along the primary visual pathway from retina through primary visual cortex are
perceptual deficits
Motion, depth, places, faces ⇒ lesion beyond the primary visual cortex
what happens if there is a cut in the optic nerve prior to the chiasm?
if it is on the right the entire right eye’s field will go dark while if it is on the left then the entire left eye’s field would go dark
what happens if there is a cut in the optic chiasm at the decussation?
the lateral parts of the visual field on each eye will be affected
- when the lateral visual fields project to the nasal area of the retina, they will not be able to cross as they usually do, but the temporal projections will be just fine
what happens if there is a cut right after the optic chiasm at the decussation prior to the LGN?
- if the cut is on the right then it will affect the lateral region of the left eye (cannot project after decussation) and it will affect the nasal region of the right eye which would temporally project back but no longer can
- if the cut is on the left then it will affect the lateral region of the right eye (cannot project after decussation) and it will affect the nasal region of the left eye which would temporally project back but no longer can
what happens if there is a cut right at Meyers loop coming from the thalamus?
- if the cut is on the right side then it only affects the top left side of each visual field
- if the cut is on the left side then it only affects the top right side of each visual field
what happens if there is a cut right across V1?
- if the cut is on the right then the left side of each visual field will be affected
- if the cut is on the left then the right side of each visual field will be affected
what are the optic tract targets? (4)
- Pretectum ⇒ luminance detection of RGCs; reflex control on pupil and lens
- Superior colliculus ⇒ responsible for eye movements
- Lateral geniculate nucleus ⇒ necessary for visual perception
- Hypothalamus ⇒ light sensing ganglion cells, so circadian clock resetting is intact in photoreceptor blindness
what is special about the hypothalamus relating to the optic tract?
it has its own photopigment and these do not go to the LGN but only the hypothalamus ⇒ nothing to do with photoreceptors
- You cannot see with the hypothalamus pathway because there is no relay to the visual cortex, but this is to train the circadian clock
T/F people with photoreceptor loss can’t train their circadian rhythms?
False, they can train them still
where does the left visual field stimulation go regarding the superior colliculus?
to the right superior colliculus via the optic nerve which then routes back to oculomotor circuitry and the extra ocular muscles
when one of the LGN neurons has small dendritic arbors, how much of a visual spatial receptor field does it have? Vice versa?
a small visual space; large space
labeled lines (V1 from LGN)
Parallel systems carrying similar information
what are the 3 types of neurons in layer 4
Magno, parvo, and koniocellular pathways
Parvocellular
specialized for fine spatial details and color
Magnocellular
specialized for flickering/moving objects ⇒ temporal resolution
T/F even though each of the two LGNs receive input from both eyes, each layer and each LGN relay cell only receives feedforward monocular input from the retina?
True
T/F Koniocellular layers are poorly understood? Layers?
True
- layers 5 and 6 within layer 4
which layers of layer 4 are mango and parvocellular cells in?
- parvo is in layers 3-6
- magno is in layers 1-2
T/F LGN cells have the same receptor fields as the retinal ganglion cells?
True
- on center off surround and vice versa
- in thalamic relay cells, something uniques goes on that we don’t see in the periphery or cortex ⇒ they can have a very unique firing pattern for the temporal form of the spikes
Temporal form
the same current injection could make the thalamic cell fire in two different modes
- LGN cells can switch their modes of firing from relay to burst mode if the LGN cell is first conditioned for ~ 100 ms to be relatively hyperpolarized and then a depolarizing stimulus is applied
Relay mode; which cells?
firing rates are carrying meaningful representations of the external world
- RGCs and LGN relay cells
Burst mode
burst firing is not carrying a meaningful representation of the external world
- In LGN only
for relay neurons what is the firing proportional to?
the intensity of the stimulus
- this is the typical firing situation
- resting membrane potential is above the dotted line in the lecture picture
what happens with burst modes? Membrane potential?
the resting membrane potential is below the dotted line where something has happened to pull the membrane potential below what it was before
The cell is hyperpolarized and some conductance has been unleashed by a voltage gated calcium channel open when the cell gets hyper polarized
T/F the same stimulus can cause a cell to fire in a burst mode where it cannot fire again after the burst period?
True
what does bursting do? What triggers it?
decouples the periphery from the sensory neocortical regions; Brainstem inputs trigger bursting and relay modes in thalamic relay cells
when does the brain have a lot of bursting? What influences AP’s?
during deep sleep
- Na+/K+ cause the action potential and Ca2+ causes the small spiking right after
- relay cells can synchronize and produce the bursting pattern
functionally decoupled
the periphery and the cortex are functionally different which does not represent what’s happening in the external world
- The intensity of stimulus is encoded by the amount of action potentials so we understand contrast ⇒ in the burst mode we lose this ability
what are other names for the primary visual cortex?
striate cortex = V1 = area 17
- The visual areas beyond the striate cortex are broadly organized into two pathway
Dorsal (MT) pathway; what lobe?
where is it ⇒ motion sensitive
- Parietal lobe, spatial vision
Ventral (V4) pathway
what is it ⇒ object recognition
- Temporal lobe
what is the V1 equivalent to the S1 homunculus?
More cortical area for the cells closer to the fovea and less going away from the fovea
- most are between 1-2 deg
Deg
degrees of visual angle from the fovea
- Foveola = 0.5 deg and fovea = 2 deg
what is special about the properties of the visual cortex?
binocular inputs in layer ⅔ and neurons become orientation selective
De novo receptive fields
emergent receptive fields in the striate cortex
- orientation tuning and stereo/depth tuning
- does not exist in LGN or retina
- Receptive fields get progressively more complex throughout the visual system ⇒ individual neurons in certain extra striate regions regions respond selectively to faces
T/F individual neurons in the primary visual cortex respond selectively to oriented edges?
True
- as the orientation of the stimulus changes, one neuron will fire preferentially to that stimulus
- There are hundreds of thousands for any given point in visual space encoding all the possible orientations
T/F the retina doesn’t respond to orientation stimuli?
False, it does respond but not preferentially to one orientation if it is a retinal ganglion cells
- cortical cells don’t respond well to a spot stimulus and respond better to elongated stimuli
in what layer of V1 do neurons have circular receptor fields? Elongated receptor fields?
layer 4; layer 2/3
- convergence of inputs accounts for orientation selectivity in cortical neurons
- 4 neurons with circular receptive fields converge (synapse) onto a single neuron in layer ⅔ to generate an elongated receptive field
T/F V1 neuron have on center off center receptor fields like the retinal ganglion cells?
True
what stimuli do layer 2/3 respond best to?
the stimulus that best drives the layer 4 cells
- The receptor fields become more fussy as you get further into the visual hierarchy
- in primates, layer 4 has receptive fields just like LGN relay cells and it is cells in layers ⅔ that have oriented receptive fields
what would you see if you only had a primary visual cortex and no higher visual areas?
You would not see continuous lines but you would see a bunch of jagged lines outlining the shape of objects ⇒ some object recognition
how does convergence work in V1?
accounts for the emergence of more sophisticated receptive fields
- LGN like circular RFs in V1 layer 4 ⇒ elongated layer 3 RFs in primates
- V2 neurons with oriented line receptive fields signal to V4 cells that respond to angles (2 line convergence)
- V4 cells signal to IT cells that respond to triangles and other elementary forms
- These IT cells synapse onto other IT cells that selectively respond to faces
IT cortex
inferior temporal gyrus for object, face, and scene recognition/perception
- The region is massive ⇒ larger than V1
- 10s of millions of neurons
- There are clusters that develop specific object recognition responses
- Some neurons encode elementary objects and others respond to something more elaborate
Fusiform face area
the medial temporal area of the IT cortex that specifically responds to faces
how did we confirm the role of IT in face recognition/perception?
having a stroke or tumor can be like a lesion ⇒ gives an opportunity to assay behaviors of what humans see
- a stroke patient had a lesion in FFA area and could no longer recognize faces but they could recognize objects
Prosopagnosia
inability to recognize faces/facial cues
what don’t FFA lesion patients struggle with?
minimal faces ⇒ eyes, nose, mouth, jawline
- They can usually draw a face but cannot recognize specific faces
- There are other parts of the IT that does object recognition but cannot put the identity of the object to a specific face
MT neurons aka MT or V5
encode the direction and speed of motion of whole objects and not just lines
- They are sensitive to global and not local motion
- intracortical processing serves to integrate and distribute elementary sensory signals in such a way that those signals can gain meaning by linkage with stored knowledge and can be acted on through motor behavior
what pathways represent distribution?
The hierarchical assembly of receptive fields is an example of integration and the what vs where pathway represent this
what happens with MT lesions?
No trouble recognizing faces and objects but cannot track the motion of any object or coordinate their own motion during action
where is the grand finale of visual perception located?
Nowhere it’s looped and distributed ⇒ visual sensation is one thing but visual perception is distributed throughout the cerebral cortex
what did patient LM confirm?
the role of MT in motion perception
- patient LM admitted to hospital complaining of extreme headaches and feelings of vertigo and as diagnosed with thrombosis of the superior sagittal sinus, which resulted in bilateral lesions of MT
- Described disorder as seeing the world in snapshots, as if sparsely sampling the frames of the movie
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