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Vision
Visible light is part of the
electromagnetic spectrum
Visible portion of electromagnetic
spectrum (380 – 700 nm
wavelength) has enough energy to
make a reversible change in
receptor molecules without
permanently damaging them.
Image formation on the retina
Retinal image is inverted and reversed. Absence of receptors at optic disc
creates blind spot in visual field about 15 degrees temporal to fixation point.
Optical defects
Myopic eye is too long, focal point
is in front of retina. Correct with
concave lens.
Hyperopic eye is too short, focal
point is behind retina. Correct with
convex lens.
Eye increases in size for 15 years.
Refractive errors decease .
Studies of experimental myopia in
primates and chickens show retina
controls growth of sclera and
length of eye by detecting image
blur. Retina can distinguish
hyperopic blur from myopic blur
though we can’t perceive
difference.
Diopter = 1/focal length in meters
Relaxed eye ~ 60 D;
Chambers, iris and lens
Anterior and posterior
chambers contain aqueous
humor. Fundus of eye
behind lens is filled with
vitreous.
Ciliary muscle + ciliary
processes = ciliary body
Aqueous humor is secreted
into posterior chamber by
highly vascularized folds,
called ciliary processes, in
secretory ciliary epithelium.
Aqueous humor and intraocular pressure
Aqueous humor is formed by
ciliary processes and enters the
anterior chamber through the
pupil. Drains from the eye at the
angle of the anterior chamber
where it must pass through
collection of tissue cords
(trabecular meshwork) before
entering canal of Schlemm.
Intraocular pressure depends on
the rate of aqueous production
and the resistance to its outflow.
Glaucoma
Optic neuropathy in which optic nerve
deteriorates with progressive enlargement
and cupping of optic disc.
There are several forms of glaucoma:
Primary open angle glaucoma. 80% of all
cases; afflicts 1% of people over 40; most
common optic neuropathy among elderly.
Often, but not always, accompanied by
elevated intraocular pressure that can stop
axoplasmic flow as nerve passes through
sclera. Structural change in trabecular
meshwork impedes aqueous outflow.
Lowering IOP does not arrest disease.
Programmed optic nerve death?
Closed angle glaucoma. 10% of cases.
Occurs when iris covers trabecular
meshwork. Causes rise in IOP to > 40
mmHg that stops blood flow to optic nerve.
IOP > 21 mmHg =
ocular hypertensive
Why is glaucomatous disk so cupped?
• Most distinctive feature of glaucoma is deeping
and enlargement of optic nerve cup. Occurs
even when intraocular pressure (IOC) is normal.
• Loss of large diameter axons (other optic
neuropathies affect mainly small axons)
• Collagen fibers of sclera form meshwork through
with optic nerve must pass. In glaucoma this
lamina cribosa bends backwards. Due to
defective collagen? IOC?
• Glia cells do not proliferate to fill gaps, resulting
from dead axons, as they do in other
inflammatory or ischemic optic neuropathies
Accommodation and Presbyopia
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Accommodation is the result
of ciliary muscle contraction.
When ciliary muscle is
relaxed, zonular fibers are
under tension and pull
outward on lens, flattening
it. Unaccommodated eye is
focused on distant objects.
When ciliary muscle
contracts, it reduces pull of
zonule fibers and lens
becomes smaller and
thicker. Due to elasticity of
lens capsule. Change
optical power 8 D.
• Primary stimulus for accommodation is retinal image blur. Changes in
image size and judgements of apparent distance can also act as stimulus.
• Presbyopia: decreased accommodation amplitude with age. From 14
Diopters at 8 years to 1 D at 50 or 55 yr. No cure. Due to age related loss of
elasticity.
The lens and cataracts
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Lens is 90% protein, more than any other
tissue in body. Transparency due to: 1)
dense, uniform packing of crystallin protein
molecules & 2) low water content
maintained by ion pumping in epithelium.
Lens is formed of concentric layers of long,
thin fibers in an elastic capsule.
Size of lens and number of fibers increase
throughout life.
Cataracts are opacities in lens. Can occur
at any age but most age related. Cause
nearly 50% of blindness worldwide. Multiple
risk factors. Dominant cause is UV radiation
which alters protein structure. Treat by
surgical removal of lens. Aphakic eye
severely hyperopic so usually insert plastic
or silicone intraocular lens
Optic disc, fovea and macula
Optic disc
Fovea
Sclera
Fovea
OD
choroid
Fovea is fixation point in central retina and
has highest acuity but low sensitivity. 1.5
mm diam. Occupies about 1 – 2 degrees
visual space. At center of macula. Macula
~ 6 mm diam.. Has good acuity and
occupies about 5 degrees of visual space.
Age-related Macular Degeneration
Progressive loss of central vision due to gradual degeneration of the
photoreceptors. First symptom is usually blurring of central vision when
reading. Usually affects both eyes. Most common cause of vision loss in people
over 55.
Causes of disease are unknown. Candidates include hereditary factors,
cardiovascular disease, smoking, light exposure, nutrition—all may play a role.
10% AMD is exudative-neovascular (wet) form. Abnormal growth of blood
vessels under macula leak blood into retina and damage photoreceptors. Rapid
progression (months). Treat with laser therapy.
90% AMD non-exudative (dry) form. Gradual disappearance of retinal pigment
epithelium over period of years. Loss of photoreceptors in affected areas.
Patient usually retains some central vision. No treatment is available.
Rod and cone outer segment
Scotopic vision:
High sensitivity; low
spatial resolution.
Starlight. Rods.
Mesopic vision:
rods and cones;
Moonlight
Photopic vision:
Low sensitivity; high
spatial resolution.
Brighter than
moonlight. Cones.
Normal vision
depends mostly on
cones.
Cones must capture 100 photons to produce response of 1 photo captured by a rod
Visual pigment
Phototransduction begins when a
photon is absorbed by visual pigment
in a receptor disk.
Photopigment contains a light
absorbing chromophore, retinal (an
aldehyde of vitamin A) coupled with
one of several proteins called opsin.
Most studies on rods where
photopigment is rhodopsin. Absorption
of photon by rhodopsin molecule
changes it from its 11-cis isomer to alltrans retinal. This triggers a sequence
of biochemical events resulting in a
receptor potential.
Phototransduction involves closing cation ion
channels in outer segment membrane
1. Absorption of photon converts 11-cis retinal to all-trans isomer
2. Activated rhodopsin stimulates G protein, Transducin
3. Activated G protein activates enzyme that breaks down cyclic GMP
4. Intracellular [cGMP] drops, plasma membrane channels close, Na+
can’t enter; cell hyperpolarizes.
Amplifying cascade: 1 photon + 1 rhodopsin hydrolyze 250,000 cGMP per second
Biochemical cascade and light adaptation
Biochemical cascade initiated by photon capture greatly amplifies signal:
Estimated that 1 light activated rhodopsin molecule can activate 800
transducin molecules. Each transducin molecule activates only 1
phosphodiesterase molecule but each of these may catalyze breakdown of up
to 6 cGMP molecules. In this way absorption of one photon by a single
rhodopsin molecule can cause about 200 ion channels to close and change
the membrane potential about 1 mV.
Light adaptation. Magnitude of amplification varies according to level of
illumination. Photoreceptors are most sensitive in dim light, less sensitive in
bright light. This prevents them from saturating and extends the range of light
intensities over which they can operate. cGMP-gated channels in outer
segment are permeable to Ca2+ as well as Na+. As illumination increases,
more channels close and intracellular [Ca2+] drops. This decrease triggers
changes in phototransduction cascade that reduce sensitivity of receptor to
light. Additional factors include neural interactions between photoreceptors
and horizontal cells.
Structure of the Retina
Direct path: Receptor – Bipolar
cell – Ganglion cell.
Indirect path: Receptor –
Horizontal cell – Bipolar cell –
Amacrine cell – Ganglion cell
Horizontal and Amacrine cells
mediate lateral interactions
Retinal pigment epithelium
contains melanin; prevents backscattering of light; essential role in
renewing photopigments and
phagocytosing photoreceptor
disks that are sloughed off and
regenerated.
From Purves et al. 2004. Neuroscience
Retinitis pigmentosa
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Common hereditary retinopathy, affects 100,000 people in U.S. RP is
group of hereditary eye disorders involving gradual degeneration of the
photoreceptors. Main symptoms are night blindness, loss of peripheral
vison, narrowing of retinal vessels and migration of pigment from disrupted
retinal pigment epithelium into retina where it forms clumps near blood
vessels.
Progressive death of rods, may be followed by loss of cones
Mutation may be X-linked or dominant or recessive autosomal gene. To
date mutations identified on 30 genes. Many encode photoreceptor
proteins. Pathogenesis is not well understood. Why do cones degenerate?
Often protein that RP affects is not expressed in cones, e.g., rhodopsin.
Dark clumps of pigment
in retina
Renewal of labeled amino
acids in rods
Normal phagocytosis of sloughedoff rod proteins by long processes of
pigment epithelium
Color vision: 3 classes of cones
There are three types of cones with
different photopigments that respond to
Short, Medium or Long wavelengths.
Individual cones are colorblind. Can’t
discriminate changes in wavelength from
changes in luminance.
S
M
L
Color perception depends on comparing
activity of ganglion cells from different
classes of cones.
Color blindness
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Trichromats (Normal)
– Most people can match any color by adjusting the intensity of three
superimposed light source producing S, M and L wavelengths
About 8% of men and only 0.5% of women are color blind
• Dichromats Can match colors with only two lights ; don’t see third color
category
– Protanopia– no red cones; x chromosome
– Deuteranopia– no green cones; x chromosome
– Tritanopia– no blue cones; chromosome 7 (rare)
• Anomalous trichromats
– Red or green gene is replaced by hybrid gene that has intermediate
spectral sensitivity. (protanomalous if it is red gene; deuteranomalous if it
is green gene that is abnormal)
Central visual pathways
Retinal projections:
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Pretectal area of midbrain
– Pupillary light reflex
Superior colliculus
– Saccadic eye movements
– Multimodal maps of visual
space
Lateral geniculate nucleus
– Cortical feedback, filters
transmission to cortex
– Part of pathway for
conscious visual
perception
Most ganglion cells go to the lateral
geniculate nucleus
Axons from nasal half of
each retina cross in optic
chiasm.
Each optic tract ‘looks’ at
contralateral visual field
Parvocellular layers
Magnocellular layers
Optic radiation to visual cortex
Lateral geniculate n.
Lateral ventricle
LGN
Meyer’s Loop
Optic
radiation
Field of left eye
Field of right eye
In left cerebral hemisphere
Calcarine sulcus
Nolte p. 434
Left visual cortex contains right half of visual
field of both eyes
Seen only by right eye
Inferior field
Calcarine sulcus
Field of left eye
Fovea
Superior field
Field of right eye
Nolte p. 436
Primary visual cortex is organized into
columns
Color sensitive regions
RE
LE
Orientation columns
Ocular dominance
columns
Visual Field Defects
Visual field of
Ophthalmic artery anurism
Pituitary tumor
Lesion in Myer’s
Loop
Visual deprivation and amblyopia
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Amblyopia is diminished visual acuity due to failure to establish appropriate
cortical connections early in life.
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Strabismus (misalignment of eyes) can cause double vision and is most
common cause of amblyopia. In some individuals brain suppresses input
from one eye which may become effectively blind. Early surgical correction
of extraocular muscle length important.
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During development, axons of cells in the lateral geniculate compete for
synaptic space on cells in visual cortex. This critical developmental
period, when cortical synapses are being formed, lasts several years in
children. Visual deprivation of one eye during part of the critical period (due
to congential cateracts, or amblyopia caused by strabismus) can result in
few cortical cells responding to the deprived eye which may become
permanently functionally blind.
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Visual deprivation after the end of the critical period when synapses for both
eyes have been established does not affect vision.
Temporal parvocellular pathway analyses
form and color
Lesions of the temporal vision-related cortical
pathway cause inability to name and identify
familiar objects, symbols, words, colors etc.
For example:
Prosopagnosia
Prosopagnosia: inability to identify familiar
faces
Lesion of lingual, fusiform and
parahippocampal gyri. Right side
only or bilateral. Caused by stroke,
tumor, demyelination or atrophy.
Cannot recognize familiar face.
Know face is a face and if sad or
happy, but not whether they have
seen it before. Cannot learn to
recognize new face.
Cannot distinguish between
members of other classes of
objects either.
Bilateral inferior occiptiotemporal lesions
Magnocellular parietal pathway analyzes
motion
Lesions of parietal vision-related cortex pathway
cause visual illusions and deficits related to the
distribution of visual attention and perception and
manipulation of items in space.
Examples:
Hemispatial or unilateral
neglect
Akinetopsia
Hemispatial or unilateral neglect
Disorder of spatially directed attention caused by lesion
of right posterior parietal region. Body centered instead
of visual field centered.
Self protraits after right posterior parietal
lesion
2 mo
3.5 mo
6 mo
9 mo
Akinetopsia: inability to detect motion
Lesion in visual area V5 (MT) in parieto-occipital cortex which
contains neurons sensitive to motion but not orientation or
wavelength. Sees moving objects but does not perceive them
as in motion.