Accurate Predictions

Your remarkable eyes

Many of us will be familiar with the facts about our eyes that we learnt in biology at school. The diagram above shows how light passes through the pupil and is focused by the lens onto the retina. The retina then sends signals to the brain, enabling us to see.

We want to look at one of the parts of the system that our biology classes glossed over. That is the way the retina converts light into electrical signals which it sends to the brain. We shall be looking at what happens in some of the components of the retina shown on the right-hand side of the digram above.

Sequence of events when light hits the retina:

light causes a molecule to change shape
the change of shape starts a complex series of chemical reactions
the chemical reactions cause a build up of electrical charge
the build up of electrical charge results in an electrical signal being sent to the brain
a second complex series of chemical reactions returns the sequence to the starting point



	No one has explained how this complex sequence could develop gradually. Have a look at the facts and see if you agree that they point to a creator.

Your Retina

When you have your eyes tested, the person testing your eyes will usually look into your
eyes. He sees the view of your retina shown on the left.

Towards the centre of the retina is the optic disc at the end of the optic nerve. The
major blood vessels radiate from the optic disc.

To one side of the optic disc is a blood-vessel-free reddish spot known as the fovea. The fovea is directed towards whatever object you wish to study most closely – this sentence at the moment.

Light entering the eye passes through the lens and is focused onto the retina.

As the diagram shows, the retina contains photoreceptor cells known
as rods and cones. Light causes a chemical reaction in the photoreceptors which results in the rods and cones sending a signal through the bipolar and
ganglion cells beneath them. The ganglion cells then send a signal down
the optic nerve to the brain.

Photoreceptor cells

We have seen that there are two different types of photoreceptor cell in the retina. The rod cells are responsible for giving the brain a black and white image. The cone cells add colour to the image seen by the brain. When light is focused onto the retina, it activates the rods and cones in the retina. There are over 6 million cones and 120 million rods in the human eye.

The diagram on the left shows a
small part of the previous
diagram and an enlarged view of
the outer segment (or light-sensitive end) of a typical
rod.

This outer segment is filled
with rhodopsin discs (1). These
discs are folded double
membranes in which the light
sensitive rhodopsin molecules are embedded (2).

Rhodopsin consists of a protein called opsin (3) and a molecule called retinal (4), which is made
from vitamin A. The retinal is situated in the middle of the rhodopsin molecule, as shown in the diagram. When light strikes retinal, it changes shape. In changing shape, the retinal forces changes to occur in the protein opsin as well.

This change in the protein opsin sets off a
series of chemical reactions. These reactions
lead to the closure of some channels in the cell
membrane that normally allow electrically
charged sodium atoms (sodium “ions”) to enter.
The photoreceptor cell then becomes more
electrically charged.

The diagram on the right shows pictorially the
complexity of the process. We shall not attempt
to explain the process in detail; the diagram is
enough to indicate the complexity. Have a look at the “Further information” section at the end for
more detail of this series of chemical reactions.

The amount of light controls the amount by which the discs are charged – more light results in a greater electrical charge. The cell then sends the corresponding signal to the optic nerve via the bipolar and ganglion cells.

By looking at the signals from the 120 million rods and 6 million cones in each eye, the brain forms the image which we see.

When the light ceases to activate a particular rod, another complex series of chemical reactions occur to return the cell to its original condition ready to be activated again.



	Your retina contains 126 million photoreceptors Each photoreceptor contains light-sensitive molecules Light causes these molecules to change shape The shape change starts a series of chemical reactions The chemical reactions cause an electrical charge The charge results in a signal going to the brain A second series of chemical reactions restores the photoreceptor to its original condition Your brain interprets the signals from the 126 million photoreceptors to enable you to see

The retina is only one part of the complex system that must be fully functional before we can see.

The challenge

The operation of the photoreceptors in the retina of our eyes gives us a challenge. That challenge is:

Did photoreceptors develop by chance, or were they created?

If we believe they developed by chance, we must explain how the system that we have considered could have developed, whilst being functional and advantageous for survival at all stages. Furthermore, we must explain how the rest of the complex systems in the eye developed at the same time – again being functional at all times.

When the theory of evolution was developed by Darwin, he was not aware of the incredible complexities that we have just looked at. Darwin explained the eye as a development from a light-sensitive spot.

The three diagrams on this page show the intermediate stages he suggested in the development of the human eye. He suggested that the human eye developed from a simple patch of photoreceptors similar to those found in a jellyfish.

An intermediate stage in the development is seen in the cupped eye
of marine limpets. The curvature of the eye blocks off the light

from certain angles so the animal can sense which
direction the light is coming from.

A further stage in the suggested development is the eye of a marine
snail, which has a simple lens to improve light recognition. It is then
argued that developments would result in the sophistication of the

human eye. In this argument the
vital question of how the lightsensitive
patch came about
remains unanswered. We have just
seen the incredible complexities of

a light-sensitive patch. For the system to work, all of the
complex chemicals must be present, in the correct place and
sometimes in the correct amount. Furthermore, the second
series of reactions, to return the photoreceptor to its original
condition, must also be in place for the system to be of any
advantage to the animal. Otherwise the photoreceptors
would cease to work after the first flash of light.

No one has suggested a plausible way that all this could have developed. This leaves us with the conclusion that there was a designer behind this incredibly complex and organised process.

Summary:

To be able to see, your brain must be able to interpret correctly the information coming from the 126 million photoreceptor cells in your eyes. No one knows how the light-sensing receptor cells in your eyes could have developed.

To be of any use the receptor cells must have:

A special molecule that changes shape when hit by light
A protein containing that molecule that correctly changes the
protein’s properties when the special molecule changes shape
Other complex chemicals that cause a complex chain of reactions
when the protein’s properties change, resulting in the buildup of an
electrical charge
A connection to the brain
The means of sending a signal to the brain which it can interpret
correctly
A system to return the receptor to its original state so that it can react
to different light conditions

The facts point to a creator

Further Information – the phototransduction cascade

For those who wish to know more, here is a more detailed description of this process. This is greatly simplified to make it understandable. (We apologise for the simplification in this description to those who know the full details of the process.) Names in italics are on the diagrams.

Rhodopsin is the complex molecule formed when the protein opsin takes up an 11-cis-retinal molecule. When a photon of light reacts with 11-cis-retinal it rearranges within picoseconds to trans-retinal and changes its shape. (A picosecond is about the time light takes to travel the breadth of a human hair.) This change in shape forces a change in the shape of the whole
rhodopsin molecule.

The change in shape of the rhodopsin (now called metarhodopsin II (meta II)) changes its chemical behaviour.

The metarhodopsin II (meta II) can now interact with another protein in the disc membrane called transducin. Each meta II molecule can interact with many transducin molecules; one estimate
says at least 500.

As the diagram shows, transducin consists of three subunits called alpha (α), beta (β) and gamma (γ). The alpha subunit has a chemical
called GDP attached to it.

The effect of meta II on transducin is to exchange a chemical called GTP for the GDP attached to the alpha subunit. This causes the alpha subunit with the GTP attached to separate from the beta and gamma subunits. So upwards of 500 alpha subunits of transducin with GTP attached have been caused by the action of 1 photon of light.

Each one of these alpha subunits then reacts with a molecule of phosphodiesterase causing its
chemical properties to change. Each molecule of this modified version of phosphodiesterase (PDE*) then destroys an estimated 4,200
molecules of cGMP in the cell.

As we have seen, a single photon can activate about 500 PDE molecules. This means that maybe 2 million (500 x 4,200) molecules of
cGMP are destroyed by the action of just one photon of light.

The destruction of all these cGMP molecules has its effect on another protein in the rod cell membrane.

This protein is called a cation
channel. The channel acts as a gateway to regulate the number of sodium (Na+) ions in the cell.

Usually this cation channel allows sodium (Na+) ions to enter the cell,

while a separate protein pumps them out again. Thus the sodium ion concentration is kept within a narrow range. When the amount of cGMP is reduced because of the action of phosphodiesterase, the cation channel closes, resulting in a reduction of the number of positively charged sodium ions in the cell. As each cation channel has to have at least three cGMP molecules to keep it open, the removal of large numbers of cGMP molecules results in a rapid closure of many cation channels in the cell membrane.

This causes an imbalance of electrical charge across the disc membrane. This imbalance of charge finally causes an electric current to be transmitted down the optic nerve to the brain via the bipolar and ganglion cells.

This, however, is only part of the process!

If the reactions we have looked at above were the only ones going on in the cell, the supply of 11-cis-retinal and cGMP would soon dry up. Something has to restore the cell to its original state so that it can react to rapidly changing light conditions. Several mechanisms are required to achieve this.

Firstly, the cation channel not only lets sodium ions (Na+) into the cell, it also allows calcium ions (Ca++) in. As with the sodium ions, the open cation channel is instrumental in maintaining the calcium ion concentration. So when the cation channel closes, the calcium ion concentration in the cell reduces. The action of Phosphodiesterase, which destroys cGMP, slows down when the calcium ion concentration falls.

Secondly, a protein called guanylate cyclase (GCAP) begins to make cGMP when calcium levels begin to fall.

Thirdly, while the previous two changes are happening, metarhodopsin II (meta II) is chemically modified by an enzyme called rhodopsin kinase (RK). The modified rhodopsin then binds to a protein known as recoverin which prevents the rhodopsin from activating any more transducin.

These three steps limit the amplified signal started by a single photon. But more processes are still required to get back to the start of the cycle. In the rhodopsin molecule, the trans-retinal eventually detaches from protein opsin and must be reconverted to 11-cis-retinal and again bound to rhodopsin to get back to the starting point for another visual cycle. The following steps do this:

1. Trans-retinal is first modified by an enzyme to trans-retinol.

2. A second enzyme then converts trans-retinol to 11-cis-retinol

3. Finally a third enzyme converts 11-cis-retinol to 11-cis-retinal and the cycle is complete.

The photoreceptor is now at last ready for the next flash of light!

We acknowledge the cooperation of the Department of Ophthalmology, University of Utah for permission to reproduce pictures and graphics from their website http://webvision.med.utah.edu