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
