Vision: retinal mechanisms Flashcards
1
Q
what are retinal cells
A
- rods, cones, horizontals and bipolars do not exhibit action potentials
- rods/cones modulate membrane potential of bipolars
- ganglion cells (& amacrine) changes AP rate, taking signal to brain
2
Q
what is the structure of the retina
A
- design flow
- photoreceptors on the outside
- light must pass through other cell structures before reaching photoreceptors - scatter
- why?
- receptors being adjacent to pigment epithelium may help to minimise reflectance / scatter
- also closer to blood supply required for high metabolic rate
3
Q
what is the foreal retina
A
- structures in front of foveal receptors are pushed to one side
- reduced light scatter / absorption, thereby increasing activity
- black pigment epithelium minimises reflectance
4
Q
what are rods and cones
A
- photopigment contained within discs of outer segment
- disks continuously migrate outwards and are regenerated
5
Q
what is the density of rods and cones
A
- no lens is perfect (including the eye)
- activity can be defined by the pointspread function
- pointspread function determines minimum separation of 2 points before they are perceived as separate entities
- density of photoreceptors in human retina precisely tuned to the pointspread function of eye optics
- lower body density - reduced acuity
- any higher of pointless: optics not good enough
6
Q
what is photopigment
A
- bleaches in response to light exposure
- human photopigment continuously bleached and regenerated
- receptors are saturated when all pigment is bleached - can no longer detect light
7
Q
what is phototransduction
A
- photopigment bleaching
- two molecules combine to form photopigment: retinal and opsin
- combined molecule (in rod cells) is called rhodopsin (‘unbleached’ state)
- light photon interacts with rhodopsin causing configurational change
- retinal and opsin part company
- cell membrane hyperpolarised (via G-protein)
- released opsin activates enzyme phosphodiesterase (PDE) (via transducing G protein)
- PDE converts cGMP to GMP (cGMP normally opens Na+ channels)
- closure of Na+ channels causes hyperpolarisation of cell because K+ continues to leak out
- neural output of ganglion cell is modified
- rod/cone hyperpolarisation results in less neurotransmitter release (glutamate)
- modulates membrane potential of bipolar cell
- change firing rate of ganglion cell (bipolar can be excitatory or inhibitory)
8
Q
what is the visible range of luminance
A
- human vision functions across ~10^15 units of luminance
- the eye can detect single photons and work in bright sunlight
9
Q
what is the difference between photopic, mesopic and scotopic vision
A
- photopic
- suited for high luminance
- cones only
- low sensitivity / high acuity
- foveal and peripheral
- mesopic
- intermediate luminance (e.g. dusk)
- rods and cones
- intermediate sensitivity / acuity
- foveal and peripheral
- scotopic
- low light vision
- rods only
- high sensitivity / low acuity
- non-foveal
10
Q
what are the mechanisms of adaptation to luminance
A
- pupil size
- switchover between rods and cones
- ‘dark adaptation’: bleaching/regeneration of photopigment
- ‘field adaptation’ (aka light adaptation: automatic gain control with photoreceptor (calcium release mechanism)
- adaptation is a constant trade off between sensitivity versus acuity
11
Q
what is the difference between rods and cones
A
- rod cells inherently more sensitive than cones, by -1 order of magnitude
- but a much bigger difference in sensitivity comes from high convergence of rods onto ganglion cells (via bipolar cells)
- degree of convergence can be altered in different light conditions
- e.g. under mesopic conditions, rods and cones may converge together
- at the extremes:
- 1 cone -> 1 ganglion cell (fovea)
- 75,000 rods -> 1 ganglion cell (periphery)
12
Q
what is the distribution of rods and cones in the retina
A
- foveal vision entirely dependent on cones
- therefore foveal acuity very poor at night
13
Q
what is dark adaptation (aka bleaching)
A
- copes with large changes in light. visual sensitivity gradually increases over ~20 minutes in dark (i.e. threshold reduces)
- photopigment progressively regenerates (following bright light at time zero)
- overall change in threshold is due to combination of rods and cones
- cones adapt faster but rods ultimately take over, since their final threshold is much lower
14
Q
what is field adaptation (aka light adaptation)
A
- very quick change in sensitivity (within seconds) when background luminance changes
- copes with fast (relatively small) changes in light
- prevents response saturation at high light
- involves an automatic gain control process
- may involve several mechanisms, but mainly due to altered calcium release within photoreceptor
15
Q
how is information processed after the photoreceptor
A
- the scenery contains a huge amount of information (130 million photoreceptors in eye)
- retinal processing partially reduces this to things of interest i.e. changes, both spatial and temporal
- this is achieved by bipolars / horizontals / amacrines
16
Q
what is the concept of a receptive field
A
- the ganglion cell is the final output of the retina
- each ganglion cell may respond to many photoreceptors
- shine a light on the retina to determine the ganglion receptive field
- some photoreceptors excite the ganglion cell, some inhibit
- forms a centre-surround shape, causing lateral inhibition
17
Q
what is lateral inhibition
A
- lateral inhibition mediated by horizontal cells
- retinal ganglion cells respond to edges
- centre-surround receptive fields: emphasise edges
18
Q
what is colour vision
A
- theoretical 1 channel receptor system
- responds purely to stimulus intensity
- one degree of freedom
- no discrimination except brightness
- a monochrome system
- theoretical 2 channel receptor system
- responds to 2 aspects of stimulus intensity
- two degrees of freedom
- can discriminate colours
- all outputs can be described by 2 numbers
- a three channel system
- fraction of light absorbed by different cones - sensitivity
19
Q
what is a colour triangle
A
- assume constant intensity (luminance) for all wavelengths
- only colour can be ‘dialed up’ by a combination of red, green and blue
- saturation: defines strength of colour (e.g. pure red is fully saturated, white is fully unsaturated)
- hue: defines the colour itself
- no wavelength can stimulate green cones alone without activating red or blue cones
20
Q
what is the neural processing of colour
A
- colour processing largely takes place in the retina itself
- ganglion cells generally don’t respond to red, green or blue alone, but in combinations
21
Q
what is colour opponency
A
- three opponent channels in retinal output
- red - green
- yellow - blue
- black - white
- may explain why yellow is perceived a primary colour
- also explains impossible colours: can have a bluish-green (turquoise) but not a yellowish-blue or reddish-green
22
Q
what is colour constancy
A
- colours tend to look the same despite large changes in the wavelength of illuminating light
- multiple mechanisms - one is adaptation. highly stimulated colour channels will tend to adapt and become less responsive
- also contextual cues (e.g. bananas are generally yellow)
23
Q
what is defective colour vision
A
- monochromats
- rod type (vv rare)
- cone type (vv rare)
- dichromats - 2 lights
- protanopes, no red, 1% men
- deuteranopes, no green, 1% men
- tritanopes, no blue, v rare both
- anomalous trichromats
- usually red or green, 6% men, 0.5% women
24
Q
what are visual pathways
A
- left visual field enters right brain
- optic nerve splits at optic chiasm
- information relayed to visual cortex via the lateral geniculate nucleus (in thalamus)
- exact location of blindness can be used to diagnose anatomical site of lesion
