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The retina and phototransduction !

  • Mechanism
  • Exam priority: medium

Light makes rods and cones go quiet; the retina turns that change into the signals the brain reads as sight.

Updated 2026-11-01

Also called: Rods and cones, Rhodopsin

See it in 3D: Retina · Macula · Optic disc · Choroid · Optic nerve

What it is

Photoreceptors work backwards from most receptors: in the dark they are depolarized and release glutamate continuously. Light isomerizes the retinal in their pigment, starting a G-protein cascade that lowers cGMP, closes cation channels and hyperpolarizes the cell. Bipolar, horizontal and amacrine cells process the signal, and only ganglion cells send action potentials down the optic nerve.

How it works, step by step

  1. In darkness, cGMP-gated channels in the outer segment let Na⁺ and Ca²⁺ in; the cell rests near −40 mV and releases glutamate.
  2. A photon isomerizes 11-cis-retinal to all-trans-retinal inside rhodopsin (or a cone opsin).
  3. Activated rhodopsin activates many transducin molecules (a G protein), which activate phosphodiesterase 6.
  4. Phosphodiesterase hydrolyses cGMP; cGMP-gated channels close and the cell hyperpolarizes toward −70 mV.
  5. Less glutamate is released: ON bipolar cells (mGluR6) depolarize and OFF bipolar cells (ionotropic receptors) hyperpolarize.
  6. Horizontal cells create centre–surround contrast (lateral inhibition); amacrine cells shape timing and motion signals.
  7. Ganglion cells convert the result into action potentials; the retinal pigment epithelium recycles all-trans-retinal back to 11-cis.

Approximate numbers

ParameterValueNote
Rods per retina≈90–120 million
Cones per retina≈5–6 millionhighest density at the fovea
Ganglion cells (optic nerve axons)≈1–1.2 millionheavy convergence from rods
Full dark adaptation≈20–40 minrods dominate after the first minutes

Approximate values for a healthy adult at rest; each laboratory sets its own ranges.

Clinical notes

  • Vitamin A deficiency (still seen in children with malnutrition) causes night blindness, Bitot spots and corneal damage.
  • Age-related macular degeneration destroys central vision (fovea) and spares peripheral vision.
  • Retinitis pigmentosa affects rods first: night blindness and a narrowing visual field.
  • Retinal detachment separates photoreceptors from the pigment epithelium, which nourishes them and recycles retinal.

Test yourself

Think of the answer, then tap the question to see it.

Why does light hyperpolarize a rod instead of depolarizing it?

Light activates transducin and phosphodiesterase, which lowers cGMP. cGMP-gated cation channels close, the inward dark current stops and the cell hyperpolarizes.

Why is visual acuity highest at the fovea?

The fovea has densely packed cones with little convergence (close to one cone per ganglion cell), and the inner retinal layers are pushed aside so light falls directly on them.

Why is night blindness the earliest sign of vitamin A deficiency?

Rods need large amounts of 11-cis-retinal to regenerate rhodopsin; with low vitamin A they cannot regain sensitivity in dim light.

What signals do photoreceptors and bipolar cells use, and where are the first action potentials generated?

Photoreceptors and bipolar cells use graded potentials and glutamate release; the first action potentials are generated by ganglion cells.

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See it in 3D

The structures of Durgical's 3D anatomy where it happens.

In Biochemistry

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Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: 14.1 Sensory Perception (OpenStax (Rice University), 2022); Anatomy, Head and Neck: Retina (StatPearls (NCBI Bookshelf), 2024); Anatomy, Head and Neck, Eye Fovea (StatPearls (NCBI Bookshelf), 2024); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 51). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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Representative model, for educational purposes only.