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Vision is our predominant sensory input regarding

the external environment.


Left Visual Field

Right Visual Field

We believe visual input above all others, leading

to sayings like Seeing is believing

Vision requires transduction of photon energy into a

frequency of action potentials in the retina of the eye
From there, the action potentials are conducted to
the primary visual cortex in the brain

The retina contains the photosensitive cells of the eye, along with
a number of other neural processing cells, and is oriented to
other structures of the eye in the following way:



Primary Visual Cortex

Left Hemisphere


Optic Nerve
Optic Chiasm
Optic Tract
Lateral Geniculate Nucleus






Circular and

Right Hemisphere

The first step in vision is to bend incoming (incident) light and

focus the photons onto the retina.
The incident photons are pieces of light that have been reflected
off of the item being viewed. Therefore, many photons are being
reflected toward the eye, and photons from one portion of the
object must be focused on one point of the retina while photons
from another portion of the object must be focused on another
point of the retina.

The cornea and lens bend the incident light, with the cornea
doing most of the bending and the lens providing fine tuning and
Original light


Incorrect bending of light results in multiple patches of retina

being activated by a single portion of the object being viewed,
leading to blurred vision.
For instance, picture looking at an arrow pointing upwards. The
light from the arrow head must be focused on retinal area, and
light from the tail on another.


Retinal image is inverted, and in focus


Light passing through the

midline (incident at 90
degrees) is not bent by the
cornea or lens


We can accommodate for near or far objects using the circular and
meridional fibers attached to the suspensory ligaments.
Contracting these fibers causes tension on the ligaments to be
reduced, allowing the lens to take on a more spherical shape. This
bends light more, enabling us to focus on nearer objects (reading).
Distant focus (gazing) is accomplished by relaxing the fibers,
which tightens the ligaments and elongated the lens - resulting in
less bending of light:
More bending of light


Less bending of light


Inserting a concave lens in front of the eye will diverge the incident
light before it is bent by the cornea and lens. This forces the cornea
and lens to bend the light more than without the concave lens, and
allows the near-sighted eye to focus on distant objects:

When the lens doesnt bend light correctly, we get blurred vision:

Emmetropia - normal vision

Myopia - near-sighted
The lens bends too strongly, focussing the image in front of the
retina because the lens cant be elongated enough. The image,
where it strikes the retina, is now blurry. Because the lens still
can bend light maximally, you can still focus on near objects.

If the lens cant bend light enough (Hypermetropia) then the

image is focussed on a plane behind the retina, again producing
blurred vision. Placing a convex lens in the light path assists the
cornea and lens in bending the light, allowing the image to be
focussed on the retina:

Myopia - near-sighted

Hypermetropia - Far-sighted

Myopia - with vision correction

Hypermetropia - Corrected vision

Distant objects are still in focus, but the assisting lens is needed for
near objects (e.g. reading)

As we age we lose some of our accommodation ability as the

protein in the lens hardens and is more difficult to change shape. At
this point we need assistance for both near and far object focussing.
This is accomplished by using bifocals:

Also with age, we may experience protein damage in the lens, and
resulting calcium precipitation. This is called a cataract, which
will block some light entry and deflect other light from its
straight line path in the lens, This results in diminished and
blurred vision.
It is corrected by removing the lens entirely and replacing it with
an artificial lens. This results in a fixed focal length for the eye.

Convex portion
for gazing

Astigmatism is another disorder of the lens. It results from a bulge

developing in one axis along the lens, and is corrected by placing
a lens with a concavity along the same axis in front of the eye:

Concave portion
for reading


We have seen that the cornea and lens are necessary for bending
light and focusing on the retina. Now, why have an iris inserted in
the light path?

This means that we must allow more light into the eye in dark
situations, and when trying to see more distant objects.

The iris acts like a shutter, allowing more or less light to reach the
retina depending on the intensity of the light source.

The pupil is the central opening in the iris, and it dilates when the
iris constricts:

Too little light and the photoreceptors will not be activated, while too
much light will activate all photoreceptors fairly evenly (such as in
snow blindness).
NOTE: We see an object because of the light reflected off of it
(reflected), or because of light emitted by the object (Luminescence).
Dark objects reflect less light toward the retina and are more difficult
to see. Similarly, light from distant objects has more time to diverge,
so fewer photons will strike our retina (even from a brightly lit
object) from a distance.

Bright or Near Object

Pupil is constricted

Dark or Distant Object

Pupil is dilated

Once the incident light is focussed on the retina, how is the
energy of the photons converted (transduced) into a
frequency of action potentials?
The retina consists of combinations of 5 primary cell types
which work together to encode incoming light.

Pigment epithelium


Horizontal Cell

Rod or


Bipolar Cell
Light path
from lens

The cell types are Rods and Cones for transduction; Horizontal,
Bipolar, and Amacrine cells for processing; and Ganglion cells
for transmission of the action potentials to the brain. The axons
of the ganglion cells become the optic nerves.

Ganglion Cell
Amacrine Cell

A schematic of the relationship is on the following page:

Optic Nerve

Rod cells are used for black and white vision, while cone cells
provide us with color vision. We will talk about how they can do
this in a few minutes.
There is a skewed distribution of Rods and Cones across the
retina. Cones, which are smaller than rods, are most concentrated
directly behind the pupil, in an area called the macula. The fovea,
located in the center of the macula, is the region of greatest visual
acuity and is predominantly comprised of cone cell transducers:
Light path




Optic disk (Blind Spot)

So, cone cells are smaller, and therefore better able to discriminate
between two separate light sources (acuity). They are
concentrated in direct line with wherever we direct our vision,
thereby giving us our greatest acuity where we direct our vision.
However, cone cells need a greater light intensity to be activated
than do rods. This means that in low light conditions they may not
be activated. You have experienced this at night when you see
something out of the corner of your eye, but when you turn your
head or eyes to stare at it you see nothing.
The blind spot that we have in our vision results from the location
where the ganglion cell axons congregate and leave the eye to form
the optic nerve. This mass of axons prevents any rod or cone cells to
be located at the optic disk, and light striking that area cannot be


Now lets look at the different functions of the retinal structures and
cells which result in our visual impression of the world around us:
Incident light

The pigment epithelium which partially encapsulates the rod and

cone cells has two primary functions.
1) The pigment absorbs photons which manage to pass by the rods
and cones without being absorbed. In the absence of pigment the
photons would strike the white sclera below and be reflected to
other parts of the retina. This could result in activation of rods or
cones outside of the retinal area where they had been focussed,
causing a sparkling -like effect when we looked at objects.

2) The pigment epithelium also stores Vitamin A (retinol).

Retinol is needed for rhodopsin synthesis by rod cells. Rod cells
use the rhodopsin for transduction of light into electrical
activity and need to constantly replace degraded rhodopsin. The
pigment epithelium provides a store for retinol, allowing rod
cells to efficiently restock their rhodopsin levels.

Such is the case with albinism, where the pigment is absent.

Wearing sunglasses decreases incident light and reduces the
sparkling effect because there are fewer photons to be reflected.

Note that a Vitamin A deficiency will result in rods not being as

effective, and these are the transducing cells that we primarily
rely on at night. Thus, a deficiency results in night blindness.


Rods provide information about general light intensity level of objects,
and are essential for night vision. The chemical that is responsible for
light transduction is rhodopsin.
Cones provide information about color, and provide us with our
greatest visual acuity. Each cone cell contains one of three photopsins.
Each photopsin is sensitive to a specific range of light wavelengths:
Green cone Red cone
Blue cone

Notice how the overlap of responsiveness of the three cone types

allows us to interpret a broad range of colors (hues). For instance,
we can specifically identify a unique color for wavelength 525 from
that of wavelength 550 by the different pattern of responses of the
three cone types:


Rod cell

(wavelength in nm)

Rods (and Cones) have

a similar structure:

40% of all Rod outer segment

cell membrane is rhodopsin.
Membrane is folded and
appears as stacks.
Many mitochondria to supply
the outer segment with ATP



Outer Segment

Inner Segment

Electrotonic connections to
horizontal and bipolar cells

(wavelength in nm)


Color blind individuals are missing one or more of the cone

subtypes, and therefore lack the ability to discriminate between as
many colors as the normal individual. Red, Green and Red-Green
are the most common forms of color blindness.


Rhodopsin is the combination of the protein Scotopsin and the
carotene derivative Retinal.
When a photon strikes rhodopsin, the retinal is converted from the
cis- to the trans- form and detaches from the scotopsin within a
few trillionths of a second. An activated intermediate in this
process, called Metarhodopsin II is the key chemical for
Rhodopsin can subsequently be reformed by the action of retinal
isomerase, which converts trans-retinal back to cis-retinal, which
reconnects to scotopsin. This process, however, takes several
minutes. Therefore, constant illumination of a rod cell causes a
decrease in rhodopsin content.

Synaptic Body


Rhodopsin is Scotopsin + cis-Retinal

Light strikes the rhodopsin


The light converts cis- to trans-retinal,

producing Metarhodopsin II


The trans-retinal dissociates, leaving behind

inactive scotopsin. Rhodopsin kinase (an
ATP-dependent enzyme) causes the

1) So, the energy in the photon of light brings about the chemical
change of rhodopsin to metarhodopsin II. What happens next?

2) The metarhodopsin II activates Transducin, a protein in the rod cell

membrane. A single metarhodopsin can activate multiple transducins,
so amplification occurs.
3) Each transducin can activate phosphodiesterase molecules.
Phosphodiesterase is an enzyme which catabolyzes cyclic nucleotides
(cAMP, cGMP).

Retinal isomerase converts trans- to cis-retinal

4) In this case, phosphodiesterase inactivates cGMP molecules,

converting them to GMP. This is also an amplification step, as a single
phosphodiesterase molecule can inactivate many cGMPs.

Rhodopsin reforms, but this requires

several minutes

Now comes the tricky part of visual transduction:

The rod cell at rest (inactive; in the dark) is chronically depolarized.

The membrane potential of -40 mV results from an elevated sodium
conductance in the outer segment. Cyclic GMP stimulates the Na
channels to stay open, so a drop in cGMP levels will decrease Na
conductance in the rod cell.
5) The drop in cGMP causes a decrease in sodium permeability in
the rod cell, causing the membrane potential to HYPERPOLARIZE.
Notice that this is the only example that I am aware of where a
sensory receptor hyperpolarizes when stimulated.
6) The hyperpolarization lasts about 0.3 seconds (300 milliseconds),
during which time the metarhodopsin has been inactivated by
rhodopsin kinase. Notice that the hyperpolarization lasts much
longer than the time required for a photon to activate the rod cell.
Well see how this hyperpolarization leads to action potentials in a
moment, but first a few important notes:

This is a part of dark adaptation (along with pupil dilation) that

provides our eyes with a 1 million-fold range of sensitivity to
light. This is a very big range.
Photobleaching is the reverse of dark adaptation: When light is
plentiful our pupils will constrict. In addition, the previous
photons striking the retina will have converted significant amounts
of rhodopsin to scotopsin (inactive). Thus, future photons are less
likely to hit remaining rhodopsin and activate a rod cell.
Test this yourself by closing one eye and staring at a light in a
dark room. Then look out into the room and switch between your
open and closed eyes. The previously closed eye will allow you to
see much more detail in the darkened room because it wasnt
Now, what happens once the rod (or cone) is hyperpolarized?

NOTE 1: Photopsins work like rhodopsin does, but they are about
300-times less likely to be activated by a photon (explaining why
they are less effective for seeing in the dark).
NOTE 2: The incident of 1 photon striking a rod cell triggers a very
rapid response that lasts for a prolonged period. A subsequent
excitation can trigger a response before the preceding one has
finished. In that case we dont see a blinking or flashing light, but a
constant image. The Critical Frequency For Fusion is how close
together in time two flashes of light need to be for us not to percieve
a flicker. This frequency is used in movies and television, such that
we see constant rather than discontinuous images.
NOTE 3: In prolonged dark, most retinene is present in the form of
rhodopsin, so the rod cell membrane is loaded with potential photon
targets and a single photon has an increased chance of being

What we need to do now is understand how the hyperpolarization

of the rod (or cone) can lead to an increase in the frequency of
action potentials in ganglion cells.
First, remember that rods and cones have electrotonic connects to
bipolar and horizontal cells. The bipolar cells then synapse on
ganglion cells, while the horizontal cells synapse on neighboring
bipolar cells. The relationship is shown below:
Rods hyperpolarize.
Therefore, so do bipolar and
horizontal cells (due to
electrotonic connections).

Ganglion cells end up

depolarizing and have APs.


How the hyperpolarization of a bipolar cell leads to ganglion cell

activation is unclear (at least to me!). The best that I have come up
with is that ganglion cells have some tonic level of activity (they
fire APs when unexcited), and that Bipolar cells are tonically active
and releasing an inhibitory neurotransmitter.
Then, when the rod (or cone) is excited and hyperpolarizes, so does
the bipolar cell. As the bipolar cell hyperpolarizes it releases less
inhibitory neurotransmitter, resulting in excitation of the ganglion
cell ( less inhibition = excitation).

Notice how a single rod (or cone) affects multiple ganglion cells
because of the presence of the horizontal cells. On the preceding
diagram we could see this effect to the left and right. Keep in mind
that the effect would exist as a circle around the activated rod. If
looking down from the top of the previous diagram, we would see a
field of ganglion cells which surround the affected rod cell:

- +- - -

+ -- +
+ +

The reduction in inhibition of the ganglion cell results in

depolarization of the ganglion cell and a resulting increase in action
potential frequency!

On-Center Field - The

ganglion cell in the center is
activated, while surrounding
ganglion cells are inhibited

Off-Center Field - The

ganglion cell in the center is
inhibited, while surrounding
ganglion cells are excited

We will focus on On-Center fields, where the lateral inhibition

provided by horizontal cells leads to inhibition of ganglion cells
surrounding the activated ganglion cell.

Now with horizontal cells providing lateral inhibition, we see the

activated center of the field is accentuated compared to the
neighboring ganglion cell AP frequency:

Why have lateral inhibition at all? It accentuates edges, and our eyes
are very good at detecting edges. In fact, our primary visual
information is encoding of the edges of whatever we are looking at.
In the absence of lateral inhibition we would have:

AP frequency

These fields are overlapping each other all across the retina,
allowing us to accentuate edges of different objects:

AP frequency





It turns out that a single ganglion cell receives input from multiple
rods or cones. All of the rods or cones influencing a ganglion cell
are encoding similar information (e.g. edges, luminosity, red, green
or blue), so a single ganglion cell is transmitting information about
only one attribute.

Most ganglion cells are transmitting edge information, some for

color and some for luminosity:
Overlapping fields
stimulated by a line
of light.
Resulting plot of action potential
frequencies in ganglion cells.

Edge information

Red information



So, the lighting information has been encoded as edges, color

components and general illumination, and is sent to the primary
visual cortex as a frequency of action potentials travelling along
specific ganglion cell axons. Also contained is information on
direction of movement within the visual field - something we are
exceptionally good at detecting.


Interestingly, edges at one angle are transmitted to one area of the

visual cortex (one cortical column), while other edge angles go
to other areas (cortical columns) of the visual cortex. Color
information is grouped by red, green or blue, and processed by
neurons which cross the cortical columns.
The bottom line: The picture is sorted by modality and cannot be
reassembled except by the visual association cortex. The
association cortex allows us to reassemble the information into a
picture that makes sense.

Cortical columns

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