Source: A Brain-Mind Odyssey, Ch. 14
Tags: vision, retina, rods, cones, rhodopsin, cone-opsin, GPCR, isomerisation, retinal, vitamin A, beta-carotene, trichromatic, colour blindness, achromatopsia, fovea, blind spot, bipolar cells, ganglion cells, LGN, visual cortex, V1, V4, V5, scotoma, prosopagnosia, blindsight, melanopsin
Vision begins when light is absorbed by photoreceptor proteins (rhodopsin in rods, cone-opsins in cones) in the retina. These proteins are GPCRs that use a light-triggered isomerisation of retinal to initiate an enormous amplification cascade. Signals pass through bipolar and ganglion cells to the LGN of the thalamus and then to primary visual cortex (V1) and beyond. Different cortical areas handle different aspects of vision: V1 (basic features), V4 (colour), V5 (motion), inferotemporal cortex (faces). Damage to specific areas produces specific deficits, from scotomas to motion blindness to prosopagnosia.
Rhodopsin
The photoreceptor protein in rod cells. A GPCR that absorbs light and initiates the visual signal transduction cascade.
Cone-opsin
The photoreceptor protein in cone cells. Three types in humans correspond to sensitivity to different wavelengths, enabling colour vision.
Retinal
The molecule embedded within rhodopsin or cone-opsin that actually absorbs light. Derived from vitamin A (retinol), which the body makes from beta-carotene.
Isomerisation (cis-to-trans)
The light-triggered change in retinal's molecular shape (from 11-cis to all-trans) that causes the opsin protein to change conformation, initiating the signalling cascade.
Trichromatic colour vision
Colour vision based on three types of cone photoreceptors with different wavelength sensitivities. Humans compare stimulation across the three cone types to perceive colour.
Scotoma
A blind spot in a specific region of the visual field, typically caused by a lesion in V1.
Prosopagnosia
The inability to recognise faces, caused by a lesion in the inferior and medial temporal lobe.
Blindsight
The ability to respond to visual stimuli without conscious awareness of seeing them. Mediated by a secondary visual pathway through the superior colliculus.
Fovea
The central pit of the retina where cone density is highest and visual acuity is greatest.
LGN (lateral geniculate nucleus)
A relay nucleus in the thalamus that receives input from the retina and projects to primary visual cortex.
The cornea, lens, and pupil focus light onto the retina at the rear of the eyeball
Fovea (also called the macula): the centre of the retina where light from the centre of the visual field is focused
Very high density of photoreceptor cells, especially cones
Best visual acuity and detail
Located where all ganglion cell axons converge to form the optic nerve and exit the eyeball
No photoreceptor cells at this point
Normally unnoticed because the brain fills in the gap
Rods: rod-shaped, very numerous, distributed across most of the retina, sensitive to very low light levels (scotopic vision)
Cones: cone-shaped, concentrated at the fovea, respond to higher-intensity light, enable colour vision
Rod cell: contains a rod-like outer segment packed with lipid bilayer membrane discs, each disc studded with rhodopsin molecules
Cone cell: similar structure but cone-shaped, containing cone-opsin proteins
Both have an inner segment (metabolic machinery) and an outer segment (light-detection apparatus)
Both rhodopsin and cone-opsins are GPCRs
The difference from other GPCRs: the activating stimulus is not a neurotransmitter but light
Retinal: the small molecule within the opsin protein that absorbs the photon
Light causes retinal to isomerise from 11-cis to all-trans configuration
This conformational change pushes on the opsin protein, changing its shape (activating it)
The rhodopsin GPCR cascade (critical for exam):
Light is absorbed by 11-cis retinal in rhodopsin
Retinal isomerises to all-trans, causing the opsin protein to change shape
Activated opsin binds to intracellular G-protein, activating it
Activated G-protein activates the enzyme cGMP-phosphodiesterase
This enzyme hydrolyses cGMP into non-cyclic GMP
Reduced cGMP concentration causes ion channels to close
The cell hyperpolarises, changing neurotransmitter release
Amplification is enormous: 1 photon → ~100 G-proteins → ~10,000 cGMP molecules hydrolysed
This is why rods can detect single photons of light
The body synthesises retinal from vitamin A (retinol), which differs from retinal by a single hydrogen atom
Vitamin A is made from beta-carotene, which is abundant in plants (carrots, lettuce, kale, sweet potatoes, tomatoes)
Beta-carotene gives carrots their orange colour
Trichromatic (humans): three types of cone-opsins with different light-absorption spectra
By comparing stimulation across the three cone types, the brain determines which wavelength of light is present
Tetrachromatic (some birds): four types of cone photoreceptors, enabling more nuanced colour discrimination
Caused by amino-acid sequence changes in an opsin protein that leave it functional but shift its absorption spectrum
Mostly X-linked: males need only one variant allele; females need it from both parents
Prevalence: ~6% of males, ~0.4% of females
Most people with anomalous colour vision do not realise their perception differs from the norm
Red-green colour blindness: loss of either L (red) or M (green) cone function
Cannot distinguish various shades in the green-yellow-red range
X-linked: ~2% of males, ~0.2% of females
Blue-yellow colour blindness: genetic variation making S cone-opsin non-functional
Cannot discriminate in the blue-green-yellow range
Very rare (<0.01%), equally common in males and females (not X-linked)
Retinal achromatopsia: complete loss of all functional cone cells
No colour experience at all; the world appears in shades of grey
Photoreceptor layer: rods and cones (detect light)
Bipolar cell layer: receive input from photoreceptors
Ganglion cell layer: receive input from bipolar cells; their axons form the optic nerve
Amacrine and horizontal cells: present in the bipolar layer; contribute to lateral processing and integration of information between photoreceptors and ganglion cells
The retina is "inverted": light must pass through other cell layers before reaching photoreceptors
Melanopsin: a photoreceptive opsin protein originally discovered in frog skin
Found in certain retinal ganglion cells in vertebrates
These ganglion cells project to brain regions involved in pupil size regulation and circadian rhythm entrainment
Separate from the conscious visual pathway
LGN (lateral geniculate nucleus): located in the thalamus (diencephalon); one on each side
~90% of retinal ganglion cell axons project to the LGN → V1
~10% project to the superior colliculus → then to higher cortical areas (V2, V4, etc.)
This alternative pathway supports blindsight
Contralateral connectivity: information from the right visual field goes to the left hemisphere, and vice versa
Visual cortical maps: the spatial arrangement of the external world is preserved topographically from retina to cortex
The receptive field of a visual neuron is the region of visual space that, when stimulated with light, changes that neuron's firing
Nearby photoreceptors respond to nearby regions of visual space
Centre-surround organisation: the centre of a receptive field excites the cell (agonist, more action potentials), while the surround inhibits it (antagonist, fewer action potentials)
This organisation is present in retinal ganglion cells
Explains the visual grid illusion (illusory shadows at intersections)
V1 lesion → scotoma: a blind spot in a specific region of the visual field
If the entire hemifield representation is destroyed → hemianopia (one entire half of the visual field is blind)
V4 lesion → cortical achromatopsia: disruption of colour perception (distinct from retinal achromatopsia, which is a receptor problem)
V5 lesion → motion blindness (akinetopsia): the person cannot perceive motion in certain regions; the world appears as a series of static snapshots
Inferotemporal cortex (IT): contains cells that respond selectively to complex features, including faces
IT / medial temporal lobe lesion → prosopagnosia: difficulty or complete inability to recognise faces
Patients with V1 damage who are blind in the affected visual field can sometimes still respond to visual stimuli they report not seeing
When forced to guess, they perform well above chance (e.g., correctly identifying the orientation of lines, detecting motion)
Mediated by the ~10% of ganglion cell axons that bypass the LGN and reach cortex via the superior colliculus
Demonstrates that the brain can process visual information without conscious visual awareness
⚠️ The rhodopsin cascade is heavily tested. Know each step: photon → retinal isomerisation → opsin activation → G-protein → phosphodiesterase → cGMP hydrolysis → channel closure → hyperpolarisation.
⚠️ Amplification numbers: 1 photon → ~100 G-proteins → ~10,000 cGMP. This is why single-photon detection is possible.
⚠️ Opsins are GPCRs activated by light, not by a neurotransmitter. This connects to the broader GPCR theme across all chapters.
⚠️ Distinguish retinal achromatopsia (loss of all cones, peripheral) from cortical achromatopsia (V4 lesion, central).
⚠️ Red-green colour blindness is X-linked (~2% males); blue-yellow is autosomal and very rare (<0.01%).
⚠️ Blindsight demonstrates a secondary visual pathway (retina → superior colliculus → cortex) that operates without conscious awareness.
⚠️ Centre-surround receptive fields explain lateral inhibition and visual illusions like the grid illusion.
Q: Walk through the rhodopsin cascade from photon absorption to change in membrane potential.
A: Light is absorbed by 11-cis retinal within rhodopsin. Retinal isomerises to all-trans, causing the opsin protein to change shape. Activated opsin binds and activates G-protein. G-protein activates cGMP-phosphodiesterase, which hydrolyses cGMP to non-cyclic GMP. The drop in cGMP concentration causes cGMP-gated ion channels to close, and the cell hyperpolarises.
Q: Why is red-green colour blindness more common in males than females?
A: The genes for L (red) and M (green) cone-opsins are on the X chromosome. Males have only one X, so a single variant allele produces colour blindness. Females have two X chromosomes and would need to inherit the variant from both parents.
Q: What is blindsight, and what neural pathway mediates it?
A: Blindsight is the ability to respond to visual stimuli in a blind region of the visual field without conscious awareness of seeing. It is mediated by the approximately 10% of retinal ganglion cell axons that project to the superior colliculus rather than the LGN, reaching cortical areas (V2, V4, etc.) without passing through V1.
Q: How does a V5 lesion differ from a V4 lesion in terms of perceptual consequences?
A: A V4 lesion produces cortical achromatopsia (loss of colour perception). A V5 lesion produces motion blindness (akinetopsia), where the world is perceived as a series of static snapshots rather than continuous movement.
Q: What is the relationship between retinal, vitamin A, and beta-carotene?
A: Beta-carotene (found in plants like carrots and kale) is converted by the body into vitamin A (retinol). Retinol is then converted to retinal, which is the molecule within opsin proteins that actually absorbs light and initiates the visual cascade.
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