Makindo Medical Notes"One small step for man, one large step for Makindo" |
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Vision begins when light enters the eye and interacts with specialized cells called photoreceptors in the retina. - π Rods: ~120 million/eye, highly sensitive to low light, essential for night vision. - π Cones: ~8 million/eye, function in bright light, responsible for colour vision and high acuity. - π― Cones are densely concentrated in the fovea for sharp central vision.
When light strikes photoreceptors, visual pigments react: rhodopsin in rods, opsins in cones. This triggers 11-cis retinal β all-trans retinal conversion β‘οΈ activates G-protein cascade β‘οΈ electrical signal β brain. Slow reconversion (all-trans β 11-cis) explains delayed dark adaptation after bright light exposure.
π Light adaptation: Dark β bright β cones activate, pupils constrict, stabilises within ~3 mins. π Dark adaptation: Bright β dim β rods need time to regenerate rhodopsin β sensitivity builds over ~30 mins.
β‘οΈ Cones adapt quickly (~10 mins), rods slowly (~30 mins). This is why sudden darkness leaves you βblindβ for a while until rods recover.
- In darkness: photoreceptors are depolarised (~ -40 mV) via cGMP-gated Na+/Ca2+ channels β βdark current.β - In light: cGMP β, channels close β hyperpolarisation β reduced neurotransmitter release β visual signal sent to brain.
- Bleaching: Light converts 11-cis β all-trans retinal β pigment inactive until regenerated. - Regeneration: All-trans β 11-cis retinal. π Cones regenerate faster (quick bright-light adaptation). π Rods regenerate slowly (explains slow dark adaptation).
The interplay between rods and cones allows us to function in both dim and bright conditions. - π Rods = night, low acuity, slow. - π Cones = day, colour, sharp. Together, they give humans a remarkable visual range across environments.