Dark Adaptation (M1) Flashcards
What are the methods for halting phototransduction?
- R* phosphorylation by rhodopsin kinase
- Interaction of R* and transducin blocked by arrestin
- Transducin inactivation by GTP hydrolysis, which is sped up by GTPase accelerating proteins like RGS9
What problems do people with defective RGS9 proteins have?
- take longer to light adapt
- hard to follow a ball in the air
- slow ERG recovery (no response to 2nd stimulus)
What is term for slow photoresponse recovery?
bradyopsia
What is the major benefit of having a phototransduction halting system?
enhances temporal resolution (can discriminate different stimuli in short period of time)
What occurs following the absorption of a photon to the chromophore and beyond?
- the chromophore (11-cis retinal) changes to all-trans retinal
- photopigment activated and transparent to light (bleaching)
- chromophore converted back to 11-cis retinal
What is the peak wavelength rhodopsin absorbs in dark adapted retinas or retinal homogenate? 1. What color does the retina appear? 2
- 500nm
2. red/brown (long-wavelength reflected back)
What is the peak wavelength rhodopsin absorbs after exposure to light with the retina looking yellow?
380nm
What is the peak wavelength rhodopsin absorbs as all-trans retinal gets converted to vitamin A? 1. What color does the retina appear? 2
- 320nm
2. white (bleaching)
What is the chromophore used by photoreceptors a derivative of?
vitamin A
What is often the initial sign of vitamin A deficiency?
night blindness
What is the disease associated with juvenile macular degeneration? 1. What is the inheritance type? 2
- Stargardt’s disease
2. autosomal recessive
What is the gene that encodes protein in rod/cone disks involved in chromophore removal from opsin? 1. In what disease has this found to be mutated? 2. What is the result? 3
- ABCR gene
- Stargardt’s disease
- toxic accumulation of chromophore-bound lipofusin in RPE and subsequent retinal degeneration
What is retinal densitometry used for?
- assess degree of bleached vs regenerated photopigment
2. map out individual cone types (with scanning laser ophthalmoscope)
What is the average percentage of S-cones of all the cones in the retina?
7-10%
What is the average percentage of M-cones of all the cones in the retina?
about 30%
What is the average percentage of L-cones of all the cones in the retina?
about 60%
What is the range of variability in the ratio of M-cones to L-cones?
1M:1L to 1M:3L
Where is the S-cones peak density? 1. Where are they missing from the retina? 2. Why are they missing here? 3
- just outside of the central region
- small center region of fovea
- maximize acuity by reducing chromatic aberrations
How long does 50% rhodopsin photopigment regeneration take? 1. Near-complete regeneration? 2
- 7 minutes
2. 35 minutes
How long does 50% opsin (cone) photopigment regeneration take? 1. Near-complete regeneration? 2
- 2 min
2. 8 min
What is the adjustment of the operating level of the visual system to lower light levels?
dark adaptation
What is the threshold difference between rods and cones on a dark adaptation curve called?
photochromatic interval
How would the dark adaptation curve be altered if a large 700nm test light was used instead of 420nm?
cone only curve would be seen because rods not effected
What happens to rod dark adaptation with age? 1. Why does this occur? 2. What disease accelerates the aging process? 3
- slows
- reduced availability of retinal
- ARMD and retinitis pigmentosa
Where is drusen located in the retina?
between choroid and RPE
What kind of cells can get regenerated chromphore from a different source besides RPE? 1. What cells provide this? 2
- cones
2. Muller cells
What does a SST-1 screen for?
diseases that affect rods (RP, Vit A deficiency, CSNB) and ARMD
Does bleaching 50% of a retina increase a threshold (makes worse) by more, less or exactly double?
much more