Receptors detected the changes in both internal and external environment .
The function of receptors is to transform the stimuli into a nerve impulse that can be sent to the central nervous system which in turn coordinates an appropriate response.
Remember all forms of stimuli are changed into nerve impulses (electro-chemical)
e.g. you taste some sugar that is dissolved in tea. The sugar is detected by the chemoreceptors on the tongue and transformed into a nerve impulse. This is the form of the information that arrives in the central nervous system.
The retina is the only part of the CNS which is directly observable (ganglion cells).
Light is coming through the eye from the right.
There are three layers of neurones shown, photoreceptors, bipolar and ganglion cells which also reflects the order of activity.
The ganglion cells and bipolar cells are transparent and do not significantly reduce the intensity of light passing to the photo receptor.
The photoreceptor absorbs the light which changes the rate of neurotransmitter produced at the first synapse (S1)
The head of the photoreceptor cell contains the light sensitive pigments.
The Bipolar cell (named after its two processes at either side of the cell body) responds by changing rate of neurotransmitter released to the Ganglion cell.
The ganglion cell generates the impulse which will travel along the axon of the ganglion to the brain. Notice that that these axons are group together to form the optic nerve. Also note that the cell body of the ganglion cell is in the in the retina.
More detail of cell types:
(a)Bipolar cell forming synapses with more than one photoreceptor.
(b) Bipolar cells connecting together rods and cones
(c)Ganglion cell collecting input from a group of photoreceptors (receptive field)
(d)Axon of the ganglion cell forming the optic nerve at (i)
(e)Summation of rod photoreceptors gives low visual acuity (resolution) Non-fovea arrangement
(f)Another form of summation
(G)The arrangement of cones in the fovea provides a high level of visual acuity (resolution).
Students should be aware that there are additional neurone layers called horizontal neurones and amacrine neurones. These are not required by the syllabus but make for interesting reading should you wish to understand the cellular basis of section E.2.5 Edge Enhancement.
The diagram above illustrates the organisation of neurones in the retina and indeed some of the difference that can be seen from one region of the retina to the next.
(e) Convergance: where 3 rods are connected to just one bipolar cell and in turn to one Ganglion cell. Therefore when interpreted in the brain it will not be possible to tell which of the receptors was activated (absorbed light). This reduces the detail in this region of the field of vision. This is typical of the arrangement of rods and other neurones in areas outside of the fovea.
(g) One cone synapses with one bipolar and one ganglion (h). The impulse traveling along the axon of the ganglion neurone can therefore be mapped (by the brain) to a precise region of the retina and therefore the field of vision. Therefore this provides detailed visual information(resolution). This arrangement is typical of the fovea where there are 1.6 X105 mm-2 cone cells. There are other species, particularly birds that have far greater densities of photoreceptors and indeed more than one fovea.
(i) Notice how the axons of the ganglion come together to form the nerve fibres of the optic nerve.
There are other photoreceptors in the retina including melanopsin in ganglion cells that seems be linked to circadian rhythm.
Consequences of the information:
Rods are used when light levels are low (dim) but they cannot produce colour vision in such conditions.
The detail provided by rods is less than the cones because of the ratio of rods to ganglion neurones.
Cones allow colour vision in humans but this is only functional when the light intensity is high.
Why would some birds of prey have double the density of photoreceptors than humans and why would they have two fovea?
Using the information already provided predict the type of retina that would be found in a nocturnal mammal.
You might find in interesting to do a quick Google on the groups of animals that have full tri-chromatic colour vision.
Are there other photoreceptive cells in the eye and what is there function if not vision?
This section of the syllabus relates to how stimuli to the eye are processed.
Edge enhancement is a ‘pre- central nervous system ‘processing of information on the retina itself. This processing is not carried out by part of the brain but by the organisation of the retinal cells.
Contralateral processing is the way in which the brain collects and integrates information from the eyes to create the perception of seeing. Both these processes require a more detailed knowledge of the retina and brain. It should also be noted that this biology is still the subject of much research and the ideas presented are hypothetical.
Stare at the square; you might notice that there is a kind of ‘white glow’ around the outside.
This glow is called edge enhancement and it results from retinal processing of information.
The purpose is to provide a greater contrast at the edges of objects.
Such ‘edge awareness' provides more detail to the visual system of the environment.
To understand edge enhancement a little more knowledge of the retina is required:
Many Rods are linked to a single ganglion cell so that the those regions of the retina organised in this way have lower visual acuity(lower resolution).
Cones tend to have a lower ratio with ganglion cells. In the fovea there may be a one to one correspondence leading to high visual acuity (higher resolution).
A single ganglion cell receives information form a number of rods and cones. The region of the retina covered by this arrangement of rods and cones is called the receptive field.
The fewer the rods and cones that supply a single ganglion the smaller the receptive field.
Small receptive fields have higher visual acuity.
The smallest receptive fields are in the fovea.
The fovea provides the most detailed information
Outside of the fovea the arrangement of rods provides an advantage in poor light since the numerous rods associated with one ganglion can gather light (summation) to generate neural activity. In poor light these regions of the retina can provide an image although the resolution will be poor.
Lateral Inhibition and Edge enhancement
A key to understanding the concept of edge enhancement is to consider the idea of lateral inhibition:
One important feature is that there are additional layers of cells not mentioned in the previous diagrams:
Horizontal cell that link photoreceptors and bipolar cells
Amacrine cells that link bipolar cells and ganglion cells
When stimulated, rod or cones may pass information to the bipolar cells and then the ganglion. The depolarisation of the ganglion cell generates neural activity in the optic nerve. However if the rod or cone cell stimulates the horizontal cell this can inhibit other photoreceptors and their ganglion cells which are further away.
The photoreceptor (rod or cone is at the top)
The bipolar neurone in black
One horizontal cell is shown
One ganglion cell
Notice that there is a one to one mapping of photoreceptor to ganglion, with this photoreceptor comes from the fovea.
Above is a schematic diagram of the fovea, each photoreceptor is being stimulated by incoming light (yellow) to pass information to its bipolar neurone and in turn to the ganglion.
However, the horizontal cells will partially inhibit the adjacent photoreceptor.
A is stimulated by bright light as is photoreceptor B, C, D, and all other photoreceptors in the image.
However the stimulated photoreceptor also stimulates the the horizontal cells which inhibit the output of adjacent photoreceptors.
Out put across the retina would be the same.
The next model takes the idea above and applies it to 'edge' when we stare at the edge of the black square on a light back ground.
(I)The dim light falls on the left side corresponding to receptors A to I.
Output from neurones A – G will be the same, a combination of stimulation by the dim light and inhibition by adjacent cells.
(III) Coming from the right. Bright light excites the neurones but there is inhibition from adjacent cells. Neural activity will be the same from L to R
(II) At the ‘edge’ H and I, will have output due to dim light but this will be overwhelmed by inhibition from the excited cells of J and even K (in bright light).
(IV) Cells J and K are excited by the bright light but they are not being inhibited by horizontal cells from the left. Cells to the left are in the dim light and the degree of inhibition is less. Hence the cell region JK will be brighter than the region to the right(L to R). The purpose of which is to increase the contrast along an edge to give better detail.
Finally let us turn to the illusion of the Hermann grid. Such illusions have provided a great deal of insight into how the eye and brain work together. The main interest of the grid are the light grey square at the intersections. Note that if you look at them directly then they disappear. How are is this illusion explained?
Lateral inhibition and edge enhancement are hypothesised as part of the process. As mentioned previously there are researchers who believe that this is insufficient to explain the phenomena
Hermann grid and edge enhancement:
The idea is that the retinal processing of information as previously described for edge enhancement sets up an illusion when looking at the Hermann grid. Presumably in the evolution of vision ‘eyes’ did not encounter 'Hermann grids' or if they did the illusion had no negative effect on the natural selection of ‘eyes’ . We might guess that the geometry of the Hermann will be so rarely encountered in nature that there has been no selection against ‘grey spot’ seeing.
When we look at one of the squares of the grid the spaces between (white lines) seem very bright. In this area the receptive fields of the fovea with their high visual acuity (resolution) are causing edge enhancement. However just out of the focus of our attention (non fovea) in the peripheral fields we are aware of the ‘grey squares’. The suggestion is that in these regions of peripheral vision:
Receptive fields are larger
The fields have lower resolution
Stimulation of the ganglion cell is a consequence of summation.
The lateral inhibition of peripheral (non fovea) receptive fields inhibits the ganglion to produce output consistent with ‘grey’ but not consistent with the degree of light falling on it in reality, it’s an illusion.
We should remember that this is scientific theory and there are alternative explanations to the Hermann grid or at least some doubt that lateral inhibition theory is sufficient to account for the Hermann grid.
Get you Photoshop or image editor going: Make a Hermann grid but change the colour of the blocks, observe and interpret.
Make the Hermann grid lines wavy, what happens, can you explain? (I can't !)
Contralateral processing is the way in which the brain collects and integrates information from the eyes to create the perception of seeing.
Stimuli from the left visual field enter both eyes.
The stimulated receptive fields of the left and right eye stimulate the ganglion cells which provide neural activity along the optic nerve.
Look closely, the left visual field information from ganglion in BOTH eyes goes to the right side of the brain.
Equally for the right visual field object, the information ends up in the left side of the brain.
The cross over point for optic nerves is the Optic Chiasm.
The optic nerves for synapses in the lateral geniculate nucleus with neurones from the primary visual cortex.
The brain is able to integrate the 2 dimensional information of the retina back into a 3 dimensional perception of the ‘real world’.
Middle ear bones (MEB)
Oval Window (OW)
Round window (RW)
Semi circular canals (SCC)
Auditory Nerve (AN)
Eustachian tube (ET)
How we perceive sound is a sequences of changes of energy from one form to another. Initially the incoming sound into the ear is in the form of a pressure wave in air which will ultimately be transformed into a nerve impulse, which as we know is a wave of sodium ions traveling down the axon.
The transformations are: