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 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

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
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.
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       IOP > 21 mmHg =
                                              ocular hypertensive
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.
   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
•   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
                    The lens and cataracts
•   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                 choroid

               Fovea           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;
Photopic vision:
Low sensitivity; high
spatial resolution.
Brighter than
moonlight. Cones.
Normal vision
depends mostly on

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 all-
      trans 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 back-
scattering of light; essential role in
renewing photopigments and
phagocytosing photoreceptor
disks that are sloughed off and

 From Purves et al. 2004. Neuroscience
                         Retinitis pigmentosa
•   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
•   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.

                                                        Normal phagocytosis of sloughed-
Dark clumps of pigment                                 off rod proteins by long processes of
in retina                                                        pigment epithelium
                            Renewal of labeled amino
                                 acids in rods
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.
              Color perception depends on comparing
              activity of ganglion cells from different
S     M   L   classes of cones.
                            Color blindness
•   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
    – 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:
                   •   Pretectal area of midbrain
                        – Pupillary light reflex
                   •   Superior colliculus
                        – Saccadic eye movements
                        – Multimodal maps of visual
                   •   Lateral geniculate nucleus
                        – Cortical feedback, filters
                            transmission to cortex
                        – Part of pathway for
                            conscious visual
          Most ganglion cells go to the lateral
                 geniculate nucleus

Axons from nasal half of
each retina cross in optic
Each optic tract ‘looks’ at
contralateral visual field                      Parvocellular layers

                              Magnocellular layers
                     Optic radiation to visual cortex
                        Lateral geniculate n.

Lateral ventricle


 Meyer’s Loop


             Field of left eye       Field of right eye             Calcarine sulcus
                    In left cerebral hemisphere           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   Field of right eye

                        Superior field                            Nolte p. 436
Primary visual cortex is organized into

                           Color sensitive regions


                                         Ocular dominance
                 Orientation columns
Visual Field Defects
              Visual field of

                                Ophthalmic artery anurism

                                      Pituitary tumor

                                     Lesion in Myer’s
           Visual deprivation and amblyopia
•   Amblyopia is diminished visual acuity due to failure to establish appropriate
    cortical connections early in life.

•   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.

•   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.

•   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: inability to identify familiar

                                              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
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.

 Hemispatial or unilateral

  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

     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.

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