Photoreception — Rods, Cones and Phototransduction

Light enters the eye through the cornea, is focused by the lens onto the retina — a layer of photoreceptor cells at the back of the eye.

The retina has two types of photoreceptors:

Fovea — the central region with only cones, giving highest acuity (detail) vision. No rods here. Blind spot — optic disc where the nerve exits, no photoreceptors.

How a single photon becomes a nerve signal:

In the dark (baseline state):

• cGMP is high → cGMP-gated Na⁺ channels are OPEN
• Na⁺ flows in → rod is partially depolarised (–40 mV)
• Rod continuously releases glutamate onto bipolar cells (inhibiting "ON" bipolar cells)

When light hits:

1. Photon absorbed by rhodopsin (a GPCR)

   • Rhodopsin = opsin protein + 11-cis-retinal (vitamin A derivative)
   • Light converts retinal to all-trans-retinal → rhodopsin becomes activated (meta-rhodopsin II)

2. Transducin (G-protein) activated by meta-rhodopsin II

3. Phosphodiesterase (PDE) activated by transducin

4. PDE hydrolyses cGMP → 5'-GMP (cGMP levels drop)

5. Low cGMP → cGMP-gated Na⁺ channels CLOSE

6. Rod hyperpolarises (from –40 mV to –70 mV)

7. Less glutamate released from rod → ON bipolar cells activate → signal to retinal ganglion cells → optic nerve → brain

Key insight: Light causes hyperpolarisation, not depolarisation. It's a double-negative — less inhibition of bipolar cells = more signal.

One photon → one rhodopsin → activates ~500 transducin molecules → closes ~200 ion channels → measurable hyperpolarisation.

This massive amplification (1:500:200) allows us to detect single photons in the dark.

When you enter a dark room from bright light:

• Bleaching: bright light converts all rhodopsin to meta-rhodopsin II (exhausted)
• Regeneration: all-trans-retinal is converted back to 11-cis-retinal (takes ~20 minutes in dark)
• Rods slowly regain sensitivity as rhodopsin reforms

Cones adapt faster (~7 min) because their photopsins regenerate more quickly — but rods provide the full dark vision.

Three types of cones with different opsins:

• S-cones (short wavelength): peak ~420 nm (blue)
• M-cones (medium): peak ~530 nm (green)
• L-cones (long): peak ~560 nm (red/yellow)

The brain compares the ratio of signals from all three to perceive colour (trichromatic theory).

Colour blindness = missing or defective cone type:

• Protanopia = no L-cones (red-blind)
• Deuteranopia = no M-cones (green-blind, most common)
• Tritanopia = no S-cones (blue-blind, rare)

• Rhodopsin = opsin + 11-cis-retinal (made from Vitamin A / retinol)
• Phototransduction cascade: Light → Rhodopsin* → Transducin → PDE → ↓cGMP → close Na⁺ channels → hyperpolarise
• Light causes hyperpolarisation (opposite to most sensory responses)
• Rods for night/peripheral, cones for day/colour/acuity
• Fovea = only cones; blind spot = no receptors
• Dark adaptation = rhodopsin regeneration (rate-limited by vitamin A availability)
• Vitamin A deficiency → night blindness (rhodopsin cannot regenerate)