Visual Physiology Flashcards
What is the cone photoreceptor divided into?
Outer vs inner, axon vs synaptic terminal
The outer segment: light sensitive. + Packed w proteins for signal transduction
The inner segment: has organelles, esp mitochondria for metabolic demand
The axon: can’t fire APs - this is as electrotonic potentials=sufficient to transmit signals as the cones are small.
The synaptic terminal: releases glut for fast, excitatory synapses!
What is the RMP of photoreceptors + why?
The RMP of photoreceptors is ~ -45 mV=v depolarised due to Na channels in the outer membrane which are open at rest
It’s a good they don’t fire APs or they’d be constantly above threshold
What happens to a cone cell at rest vs when light hits it?
At rest, the cell constantly leaks glutamate into the synapse
However, when light hits the outer segment, some Na channels close -> hyperpolarises the cell - Less glutamate is leaked as a result!
When light decreases, more Na channels open =depolarise, more glutamate released
Photosensitive proteins (photopigment) are in the outer segment membrane layers
Describe this photopigment and how it is activated
In the photopigment, opsin is bound to retinal
In retinal, all C=C are trans apart from cis bond at position 11
Cis bond is less stable; it ruptures when light hits the photopigment and then reforms in the trans position
The light-mediated conversion from retinal to all-trans retinal activates photopigment→ stimulates G-protein pathway→fall in [cGMP]→ closes Na channels →hyperpolarise
What happens right after photopigment is activated in response to photons?
Why does this happen?
Response to a single photon must be brief, so it must be terminated quickly. If it persisted, we’d get a trail of after images
The photopigment is deactivated + Used retinal is removed and recycled back to 11-cis-retinal
G-protein activation stops and cGMP levels are restored!
Another 11-cis-retinal attaches to the opsin, ready when the next photon hits again
How are we adapted to respond to photons and what can happen if this goes wrong?
Adaptation makes each photon more effective in the dark and less effective when bright.
Mutations of proteins involved in this adaptation –> degenerative disease
Retinitis pigmentosa = mutation which causes destruction of the RPE, which causes blinding! + it involves >60 known genes
Photoreceptors depolarise and hyperpolarise v fast to enable super quick response
This speed comes from high resting metabolic activity
What does this signify?
High resting metabolism needs energy/ good blood supply - most tissues have a dense capillary bed to achieve this
The receptors must be closely packed as possible to sample the visual field effectively, therefore a capillary network isnt ideal as it would disrupt packing
3 ways photoreceptors (PR) receive good blood supply?
Rapid oxygen and nutrient supply from the choroid
Also a fast BF through large leaky vessel walls -> this helps maintain arterial PO2 across the Outer retinal layers!
The outer PR segment (furthest from the light) is in contact w the RPE -> This forms the blood-retinal barrier
Describe 5 features of retinal pigment epithelium
Form of glial cells:
Has long projections that holds the retina in place
RPE helps remove fluid from around the photoreceptors
RPE cells act as the blood retinal barrier- controls what enters/leaves the retinal cells
All-trans retinal reforms into 11-cis retinal here
RPE cells act as phagocytes + renews the outer photoreceptor segments every 10 days
What can happen to RPE if there is a tear in the retina?
RPE normally removes fluid from extracellular space around the photoreceptors
However, a tear in the retina causes excess fluid to move into this extracellular space
This overwhelms the capacity of the RPE to remove the fluid → causes RPE + photoreceptors to separate, and the Neural Retina ‘floats off’ !
What is age related macular degeneration?
Inflammatory, fatty plaques (drusen) come from the blood in the choroid, or from photoreceptors themselves + sit within the Pigment Epithelium
The plaques prevent supply of nutrients from reaching photoreceptors -> photoreceptors die!
Each cone cell provides inputs to several types of ganglion cell
What are these 4 types of these ganglion cells?
Off cells: excited by less photoreceptor illumination
On cells: excited by more photoreceptor illumination. An inhibitory synapse inverts the response
Parvocellular cells: fine detail + red-green colour. Small RF
Magnocellular cells: for fast movement + broad outlines. Large RF
Explain how parvocellular cells allow us to see in fine detail, eg when there is less light
Less light: photoreceptor depolarisation releases glut. This excites a Bipolar cell→release glut→excites Parvocellular cell + it fires APs
The centre of the parvocellular RF is excitatory. The surround is inhibitory - therefore more widespread light will depolarise the inhibitory interneurons, inhibiting the Parvocellular cell
therefore a difference in excitation + inhibition= allows P cells to see fine detail! (we see the contrast)
how do we see different colours?
Blue, green and red cone photoreceptors?
The ? of the response will be the ? of the colour
? cells compare the ? - the difference allows us to ?
We also compare the combined ? with ? cones, but this comparison is carried out by ?
The size of the response will be the same no matter the wavelength or intensity of the colour
Parvocellular cells compare the ratio of Red: Green cone activation - the difference allows us to identify the wavelength!
We also compare the combined Green + Red (yellow) output with blue cones, but this comparison is carried out by a pure colour pathway
What does the retina & LGN encode VS the primary visual + visual cortex?
The retina and LGN encode: Contrast (edges of things) + Wavelength (colour)
Cells in the PVC also encode: Orientation of edges, presence of corners , Direction of motion + Binocular disparity (allows 3D vision)
3 functions of inferior temporal lobe?
What happens if there are lesions in this pathway?
What influences our depth perception?
Inf. temporal lobe: responsible for recognition + receives Parvocellular input to extract fine details
Lesions in this pathway ->Associative agnosia: pt can see an object/faces, but it has no meaning!
Inf temporal lobe also perceives depth
Image orientation influences our depth perception - e.g: A long, thin rectangle appears to have more depth than one of the same size that is short and fat
Most eye movements we make are reflexive saccades. What are these?
Reflexive saccades: no higher cortical input - happens reflexively in response to something entering our visual field
Retina -> Superior colliculus →activates horizontal + vertical Gaze centre nuclei -> CN nuclei -> extraocular muscles - eyes jump to see what has entered visual field
What are Exploratory saccade movements? Explain the pathway in the brain as well.
Exploratory saccades explore an image for Fine detail
Parietal Cortical inputs direct where we look within the Broad image outline -> Superior colliculus (red star)
green= vertical gaze centre
pink= horizontal gaze centres
What are voluntary saccades?
Voluntary saccades: voluntarily flick our eyes across to look at something (e.g. a clock)
Conscious decisions feed into Frontal eye fields + Spatial info feeds in thru Parietal cortex –> Superior Colliculus
Pink= horizontal, green= vertical gaze centres
Smooth pursuit eye movements?
Smooth pursuit: focuses on + follows an object, which must be fixed in the Fovea
Spatial input from Parietal cortex -> Frontal eye fields -> Pontine nuclei→ Vestibular nuclei via the Cerebellum
The vestibular nuclei account for Head Movements before activating the extraocular muscles
Complete the table to compare all of the conjugate eye movements
What are the 2 pathways which occur simultaneously for converging of the eyes?
Pretectal nucleus activates both oculomotor + Edinger-Westphal nuclei
Oculomotor activates CN III –> contracts Medial rectus, converging the eyes.
At the same time, Edinger-Westphal nucleus activates parasymp short ciliary nerves, which causes:
Accommodation for close vision
Pupil constriction to allow better focus
what can patients with occipito-parietal lesions see + name of this?
occipito-parietal lesions cause simultagnosia
compare functions of inferio vs superior temporal areas in eyesight?
Inferior temporal:
What shape and colour is it?
What is the depth of the image?
What is it + What does it mean?
Superior temporal:
Is there movement in the retinal image?
Is this due to object or self-movement?
Where is the object going?
