Eyes 4 Flashcards
duplicity theory
our eyes adjust to seeing in the daytime (Photopic vision) and at nighttime (Scotopic vision). At a mid range of luminance, both rods and cones are working (Mesopic vision)
dark adaptation
First move into the dark:
Cones not working – not enough light
Rods not working – Rhodopsin was bleached and cannot be used right away
Move from a well lit area into a dark area.
why ships red lights
Rods are blind to Red light, red wavelength is not captured by rhodopsin, therefore will not bleach them. Use cones to detect red light
light adaptation
All Cones and Rods instantaneously stimulated and photopigments are bleached, causes flood of signals to the brain and is seen as a bright glare and you can’t see.
After only few seconds to 60 sec, cones desensitize and adapt (reset time before can fire again) and you can see again. Cones are faster to recover from bleaching than rods. Cones also require more energy to become bleached.
Rods unable to function because Rhodopsin is bleached
Young-Helmholtz Trichromacy Theory of color vision -
brain assigns color based on the proportion of nerve impulses from each cone type: blue, green, and red cones.
opponent process theory
After cones, ganglion cells send signals to the brain in three types of opposing color channels (Blue+Yellow, Red+Green, and Black+White)
Final stage to color perception occurs at the
cerebral cortex
dichromats
(2% of men) one of the three cones pigments is missing so color is reduced in two dimensions red- green colors or blue-yellow. Red-Green most common.
(Protanopia) –
no red cones, so red appears grey
deuteranopia
(Deuteranopia) – no green cones.
Red and Green pigment genes are on the X-chromosome, mutations more common in males than females.
(Tritanopia) –
no blue cones, blues appear greenish, yellows and oranges appear pinkish, and purple color appears deep red. Blue pigment gene is on chromosome 7, so equal in males and females (rare).
Anomalous trichromats
(6% of men) – one of the three cone pigments is altered in its spectral sensitivity, not missing so poor red-green hue discrimination.
Monochromats
(0.001% of population) – two cones or all three cones not functional – no color vision at all, see only black, white, and greys
Information about where light is, what’s moving, where borders are, etc. processed by
retina, sent through optic nerve
Hits LGN (Lateral Geniculate Nucleus) in the thalamus, then relayed to Primary Visual Cortex (V1) in the Occipital lobe
phototransduction in rods
Analogous to activity at G-protein coupled neurotransmitter receptor - but causes a decrease in second messenger
Light energy changes shape of pigment molecule in membrane
Shape change activates G-protein, which reduces production of second messenger
Na+ channels closed
dark current
Rod outer segments are depolarized in the dark because of steady influx of Na+
Photoreceptors hyperpolarize in response to light
phototransduction
Rod pigment rhodopsin absorbs light, changes shape
G-protein (transducin) stimulated
Turns on enzyme phosphodiesterase (PDE), which breaks down cGMP
Reduction of cGMP causes Na+ channels to close, membrane hyperpolarizes (Na+ stuck outside)
signal amplification
each pigment activates many g-proteins, each g-protein activates many proteins, etc. (we can detect a single photon because of this!)
dark adaptation factors
Dilation of pupils
Regeneration of unbleached rhodopsin (going into dark)
light adaptation
temporarily saturated upon entering bright light from dark
Cones hyperpolarized immediately, but membrane will gradually depolarize to -35mV thanks to Ca2+
