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Report 2

[edit] Introduction

I initially intended to create this as an entirely new report, but seeing as how report 2 was very detailed I decided to base this one on it. Notable changes are more detailed analysis of the retinal circuitry, as well as a much more thorough understanding of the LGN.

[edit] Purpose

To gain a better understanding of the LGN which will ultimately be my area of specialization. I am currently considering investigating the temporal ancoding algorithms of the LGN. I would need to explain why P cells and M cells would have to be independently dealt with.

[edit] Retina

Light is concentrated from the eye and passes across these layers (from left to right) to hit the photoreceptors (right layer). This elicits chemical transformation mediating a propagation of signal to the bipolar and horizontal cells (middle yellow layer). The signal is then propagated to the amacrine and ganglion cells. (Modified from a drawing by Ramón y Cajal.)

The retina is primary location of light processing by the rods and the cones. It has 6 groups of neurons, roughly 55 types of neurons and 10 layers, from outermost to innermost, the important 3 are:

1. Photoreceptor layer - Rods / Cones
2. Inner nuclear layer Bipolar Cells,Horizontal Cells,Amacrine Cells
3. Ganglion cell layer - Ganglion Cells (gives rise to optic nerve fibers).

Although all three layers are composed of neurons, only the amacrine cells and the ganglion cells fire action potentials, the photoreceptors, bipolar cells and horizontal cells generate local graded potentials. The process of generating graded potentials will be discussed in the next section

[edit] Photoreceptors

The photoreceptor has three segments: an outer segment, and inner segment, and a synaptic ending.

1. The outer segment absorbs light by visual pigments which are arranged into disks.
2. The inner segment contains the nucleus, ion pumps, transporters, ribosomes, mitochondria, and endoplasmic reticulum
3. the synaptic terminal releases glutamate and recieves synaptic inputs.

The process whereby light shining onto the retina is used to change a membrane potential, and generates local graded potentials, is called phototransduction and it proceeds as follows

1. Inactivated (in the dark) sodium ions move into the cell and depolarize it to about -40 mV (from -65 mV)
2. In the presence of light, opsin on the outer segment of the photoreceptor absorbs a photon
3. This leads to several intermediary steps, and the sodium gates are closed
4. In the absence of sodium the photoreceptor hyperpolarizess
5. Hyperpolarization ensures less relase of neurotransmitter glutamate

The inhibition of glutamate, which can either excite or inhibit postsynaptic bipolar cells, ensures that there are now a pool of bipolar cells that are either hyperpolarized or depolarized. It is interesting to note that the presence of light actually reduces the photoreceptors response rate. Also as a note, photoreceptors do not signal colour or light intensity, only the presence of light.

[edit] Cones

Cones are primarily found in the centre of the retina (fovea) and act to distinguish light and other features present under normal lighting conditions. As would be expected, there are three different types of cones; short cones (S) react best to blue colours, medium cones (M) react best to green colours, and long cones (L) react best to red colours. The cones synapse directly onto bipolar cells and/or horizontal cells. The L and M cones are unique in that their optimal wavelengths are so similar. It has been suggested that the L and M cones arrived later on in the evolutionary cycle, long after the rods and the S cones.

[edit] Rods

Rods are found in the periphery of the retina and are primarily used at night, and they outnumber cones twenty to one. They exist in only one form, and they drive only a single type of bipolar cell, and they furthermore synapse only to a special type of amacrine cell (AII). This is due to the fact that they formed after cones did (in the evolutionary timescale), therefore, they probably piggy-backed on the existing cone circuitry.

[edit] Amacrine, Horizontal and Bipolar Cells

Although the connections in the retina are complicated, they follow this general layout:

• Photoreceptors connect to bipolar cells
• Horizontal cells connect photoreceptors together
• Bipolar cells connect to ganglion cells
• Amacrine cells connect bipolar cells together
• Ganglion cells converge to form the optic nerve

[edit] Bipolar Cells

Bipolar cells receive their input from either rods or cones, but not both, and they are called rod bipolar cells, or cone bipolar cells, respectively. The photoreceptors, on the other hand, are not dedicated to any single bipolar cell, they are instead tapped by a large number of bipolar cells. The mamallian retina has about 12 (Masland) different types of cone bipolar cells. Hyperpolarizing bipolar cells (ones which hyperpolarize with reduction of glutamate) have an off-centre receptive field (since shining a light on its receptive field causes it to hyperpolarize). Depolarizing bipolar cells (ones which depolarize with reduction of glutamate) have an on-centre receptive field (since shining a light on its receptive field causes it to depolarize). Bipolar cells can also be designated Midget or Diffuse. Diffuse bipolar cells make connections to multiple cones, whereas the midget bipolar cells connect to only one cone. By the this stage we begin to see the earliest stages of center-surround inhibition, brought on by horizontal cells (see below). Also, h bipolar cells and d bipolar cells are about equal in numbers, and, like amacrine cells, outnumber ganglion cells five to one.

Diffuse bipolar cells receive inputs from both M and L cones indiscriminately, and as of yet, no significant S cone input has been observed.

[edit] Amacrine Cells

Amacrine cells make inhibitory synapses on the axon terminals of bipolar cells, thus controlling their output to ganglion cells. Furthermore, amacrine cells outnumber horizontal cells four to ten times over, they make up 40 percent of all neurons in the inner nucleus layer and they display the most diversity of the retinal cells, existing in around 30 forms (Masland). Amacrine cells also seem to account for the corelated firing amongst ganglion cells, and it has been suggested (Masland) that the amacrine cells are responsible for distinguishing object motion from background motion. Amacrine cell types play much more specific roles then horizontal cells (the other intermediary retinal cell) since they connect certain types of bipolar cells (for example the ON signal of a rod H bipolar cell) to a certain type of ganglion cell. They can be calssified into two groups, based on whether they fire action potentials, or generate local graded potentials.

[edit] Horizontal Cells

Horizontal cells are interneurons that provide lateral inhibition, like amacrine cells, and they are connected to other horizontal cells via gap junctions. Horizontal cells are like H bipolar cells in that they hyperpolarize in the presence of glutamate, and they are the least diverse of the retinal cells existing in one of only 2 (Masland) forms; HI and HII. HI cells do not discriminate between S,M or L cones, whereas HII cells tend to give a large response to S cone stimulus, which is interesting since S cones account for only 10% of the total cone population. In sum, the horizontal cells are capable of selectively seeking out or avoiding S cells, however, they are indiscriminate towards M or L cells. In addition to this, all three inputs are hyperpolarizing, therefore the horizontal cells are incapable of performing spectral opponency. It is for this reason, that it is believed that spectral opponency is carried out by the amacrine cells.

When photoreceptors are illuminated they hyperpolarize and the horizontal cell reduces the release of GABA, which has an inhibitory affect on the photoreceptors. This reduction of inhibition leads to a depolarization of the photoreceptors. We therefore have the following negative feedback

Illuminationphotoreceptor hyperpolarizationhorizontal cell hyperpolarizationphotoreceptor depolarization

One proposed theory for facilitation by the horizontal cells proceeds as follows. Assume we have 11 photoreceptors, one H bipolar cell, and one horizontal cell. All ten photoreceptors connect to the horizontal cell, and the middle photoreceptor (P_m) connects to the bipolar cell. The surrounding cells, which represent the outer receptive field, will be designated P_o Then we can explain an off-centre arrangement as follows. If light is shown onto the P_m then

1. P_m is activated by light and therefore hyperpolarizes
2. P_m reduces release of glutamate
3. Reduction of glutamate hyperpolarizes the H bipolar cell
4. Reduction of glutamate hyperpolarizes the horizontal cell and it reduces release of GABA
5. Since P_ois still releasing glutamate, reduction in GABA is marginal

If the light is shown onto the surrounding area then

1. P_o is activated and therefore hyperpolarizes
2. P_o reduce release of glutamate
3. Reduction of glutamate hyperpolarizes the horizontal cell
4. Horizontal cell reduces release of GABA
5. Reduction of GABA depolarizes photoreceptors
6. P_o not affected since they are strongly being hyperpolarized by activation
7. P_m is affected and therefore depolarizes
8. P_m releases glutamate
9. H Bipolar cell is depolarized

To explain diffuse light, then we consider both cases together, and as it turns out, the two effects cancel each other out, and we get little to no affects. This fits nicely with the model put forth in From Neuron to Brain whereby the ganglion cells respond to a center surround inhibition.

[edit] Ganglion Cells

The left receptive field of the ganglion cell shows that it will be activated if the light is concentrated on its center, and it will be inhibited by light shining on its outer receptive field. The right image show the opposite case

The last layer in the retina, which collects to form the optic nerve is the ganglion cell layer. There are about 12 (Masland) different types of ganglion cells, and a total of 100 million photoreceptors converge to only 1 million of them, therefore, a good deal of encoding has taken place. When one looks at the receptive field of a ganglion cell, the area of the retina from which a ganglion cell’s activity can be influenced by light, it becomes apparent that it is more sensitive to differences within the receptive field than light intensity. On-centre ganglion cells will become excited if light is shone onto the centre of their receptive fields, and likewise off-centre ganglion cells will become excited when light is shone onto the outside of their receptive fields.

Depolarizing on centre cone bipolar cells connect with corresponding on centre ganglion cells. Also, hyperpolarizing off centre cone bipolar cells connect with corresponding off centre ganglion cells. Consequently, a change in membrane potential of the bipolar cell, causes a change in the membrane potential of its ganglion cell in the same direction. Surprisingly, rods and cones of the same area of the retina, supply the same ganglion cell but by different means. The rods indirectly connect via the rod bipolar cell-AII circuitry which finally connects to the ganglion cells. Although all ganglion cells recieve input from cone bipolar cells, most of their inputs come from amacrine cells (about 70%)

The ganglion cells can be loosely grouped into P and M categories, which gives rise to the parallel processing in the visual pathway. The P ganglion cells project to the four dorsal layers of the LGN, and they have small receptive field centres, high spatial resolution, are sensitive to colour, and provide information about fine detail at high contrast. The M ganglion cells project to the larger cells in the two ventral layers of the LGN, have larger receptive fields, are more sensitive to small differences in contrast and to movement, they fire at higher frequencies, and conduct impulses more rapidly along their larger diameter axons.

Amazingly, the ganglion cells neglect almost ninety-nine percent of the information presented to them by the photoreceptors. They do not convey absolute levels of illumination, because they behave the same at different background levels of light, it appears that they measure differences between their receptive fields by comparing the degree of illumination between the centre and the surround of their receptive fields.

Midget Ganglion cells are believed to form the red-green opponent pathway.

Bistratified ganglion cells are believed to form the blue ON-yellow OFF pathway. However, in this case, it is not a center-surround organized, just an overlap of the two.

[edit] Lateral Geniculate Nucleus

The optic nerve projects onto a structure called the Lateral Geniculate Nucleus. The LGN is structured such that it has a left and a right hemisphere, within which there are six distinct layers. Layers 2, 3 and 5 receive their inputs from the ipsilateral eye (w.r.t the left or right hemisphere) whereas layers 1, 4 and 6 receive their inputs from the contralateral eye (w.r.t. the left or the right hemisphere). There are roughly 1 million cells in the LGN, however, the optic nerve fibres diverge to connect to multiple LGN cells, as opposed to a simple one to one mapping. Not only are the cells topographically ordered (neighbouring ganglion cells project to neighbouring geniculate cells) but they are retinotopically registered along the different levels. Therefore, if a sample rod is taken tengentially from layer 1 to layer 6, we will hit the same receptive fields, alternating between one eye, and the other. Suprisingly, retinal input accounts for only 30% of the input to the LGN, with the great majority coming from V1. Historically the layers are numbered from the bottom up, and layers 1 and 2 have the larger, and much faster cells.

An interesting observation pointed out by Blitz is that ganglion cells which synapse onto interneurons in the LGN cause inhibition that spreads onto thalama-cortical (TC) neurons beyond those connected to it. Perhaps I can propose a model for the K layers in the LGN

[edit] Receptive Field

The receptive fields of adjacent neurons overlap since neighbouring regions of the retina make connections with neighbouring geniculate cells. This overlap means that the receptive field of the LGN is even more scrutinous when it comes to diffuse light than is the ganglion receptive field. This is because the contrast mechanism is more finely tuned by more equal matching of inhibitory and excitatory areas. Therefore, whereas the ganglion receptive field does somewhat respond to diffuse light, the LGN receptive field is very poor at responding to diffuse light.

[edit] Magnocellular Layer

These M cells, in layers 1 and 2, work much faster, however, they do not process as much information. The M cells are the largest, and they are the most ventral, therefore, they are closest to the optic nerve.

[edit] Parvocellular Layer

The P cells, in layers 3 to 6, are much smaller and slower, but come with the added advantage that they can do complex calculations such as colour detection.

[edit] Koniocellular Layer

Between each of the M and P layers lies a zone of very small cells, the K cells.

[edit] Function

It has been pointed out by Dong&Atick that the retina only removes spatial correlation from the visual input, and delivers an encoded signal which is temporaly redundant. They propose that the LGN's role may be to reduce temporal correlation and complete the spatial-temporal decorrelation process

[edit] Lagged and Non-Lagged Cells

The geniculate cells can be classified, based on their responses, into two groups, and, based on their input, further into two groups, for a total fo four groups. The input arriving from the geniculate cells can be designated one of two spatial categories, 'on' or 'off'. The output can be designated one of two temporal categories, 'lagged' or 'non-lagged'. Generally geniculate input is dominated by one category, therefore, we need not concern ourselves with a third case where both on and off input compete. The on cells recieve their input from on-center cells, and likewise for the off cells. The Lagged cells represent the temporal group which exhibits a decrease in luminosity over time, and the non-lagged cells represent the temporal group which exhibits an increase in luminosity over time. We therefore get the following four groups:

1. On-Lagged: a decrement of light and on-center
2. On-Non-Lagged: an increment of light and on-center
3. Off-Lagged: a decrement of light and off-center
4. Off-Non-Lagged: an increment of light and off-center

[edit] Visual Cortex

One proposed situation for simple cells. The three overlapping cells from the LGN are only activated when a bar of a certain size and orientation hits that particular receptive field

The LGN eventually projects onto one of the six layers of the primary visual cortex (aka V1), but mostly onto layer 4. From here information is passed onto V2, V4 and MT, and finally Inferotemporal and Parietal 7. It is important to note that both hemispheres of the visual cortex are symmetric, and they simply receive their inputs from the respective LGN hemisphere. As is the case for the other areas of the cortex, the visual cortex has 6 distinct layers. The visual cortex is much more complicated than the LGN or the retina because it has many more cells, many more horizontal connections, and although it has all of its inputs feeding in from the LGN, it is difficult to predict where that information streams out to, therefore it has, as present, an unknown bandwidth. It is known, however, that only twenty percent of the neurons are intrinsic (accept incoming info?), the other eighty percent project to other parts of the brain, possibly within the neocortex. Conservative estimates place the number of different types of neurons in the cortex at around 1000 (Masland)

[edit] Simple Cells & Complex Cells

There are three subgroups of cells within the cortex: Simple cells, complex cells, and complex cells with end inhibition. The simple cells respond only to a bar of a certain size, and oriented at a certain angle. The complex cells on the other hand can detect edges of any size and/or orientation. Complex cells can also detect corners, in which case we label them with end inhibition. It may be the case that an array of simple cells could connect to a complex cell to give rise to its behaviour. To illustrate this point, consider the case where a complex cell has a receptive field of that of 100 simple cells (10x10 plane) and for each 'cell' it has four simple cells oriented at 90 degrees to each other. Then with 400 simple cells, the complex cells can react to a whole host of bars, in one of four positions, anywhere along its receptive field. If we consider a complex cell with 3600 simple cells, then it can distinguish bars of any orientation every ten degrees. Throughout the entire mammalian visual stream, one will find that there is a great deal of hierarchies and precise stratification, the visual cortex is no exception.

Proposed diagrom for complex cells, through use of simple cells. As is clear, a complex cell can distinguish between edges anywhere on its visual field, and generally of any size. By extending the same arguement, one can show how the complex cells can detect edges.

[edit] Ocular Dominance Columns

An interesting formation within the visual cortex is that of Ocular Dominance Columns (ODCs). Horizontally along the layers of the cortex, there exist strips which are entirely controlled by one eye or the other, but not both. It has been suggested that activity dependent competition causes the formation of ocular dominance columns. The columns are 250 to 500 μm wide, and taking the soma to be from 4 to 100 μm wide, that means that every column has about 5 to 75 neurons.

[edit] Orientation Columns

Not suprisingly, if one samples the cortex perpindicular to its surface, one we encounter similar orientation preferences amongst the neurons. The columns here are much more percise than ODCs as these are on average only 20 to 50 μm wide, which means that there are less than a dozen neurons in each column. When the a map of the OCs are superimposed with a map of the ODCs it can be seen that where the ODCs meet, OCs cross perpindicular to the two ODCs. This makes sense since the neurons for both eyes in that area should have the same orientation preference.

[edit] Color Vision

An antagonistic red-green receptive field. This piggy backs onto the antagonistic center surround receptive fields of the ganglion cells. Here we have an excitatory red center with an inhibitory green surround. If a red spot was on a greed background, they would cancel eachother out

Color perception occurs by comparing two (or more) different types of cones. Within the retina the S,M, and L cones combine antagonistically to form red-green and blue-yellow spectral opponent pathways. Within the red-green pathway signals from L and M cones are opposed. Within the blue-yellow pathway signals from S cones oppose combined signals from L and M cones. It has been suggested that color coding could piggyback the antagonistic center surround organization that exists in ganglion cells. One way to do this would be to have the center be excitatory towards one cone (say L) and the surround be inhibitory to another cone (say M); we then get the situation whereby the center responds to red, and the surround responds to anything besides green. Therefore, the signal generated would be greatest to a red spot on a blue (or neutral) background.

[edit] Visual pathway

Because of the complex nature of the visual system, and the burden of pure parallel processing, it is quite difficult to trace the exact pathways in the visual system.

[edit] References

Blitz, Dawn M (2005). "Timing and Specificity of Feed-Forward Inhibition witih the LGN". Neuron 45: 917-928. 

Boycott, Brian (June 1999). "Parallel Proccessing in the Mammalian Retina". Ivestigative Opthalmology & Visual Science 40: 1313-1327. 

Dacey, Dennis M (1996). "Circuitry for Color Coding in the Primate Retina". Proc. Natl. Acad. Sci 93: 582-588. 

Dacey, Dennis M (1999). "Primate Retina: Cell Types, Circuits and Color Opponency". Progress in Retinal and Eye Research 18: 737-763. 

Dan, Yang (1996). "Efficient Coding of Natural Scenes in the Lateral Geniculate Nucleus: Experimental Test of a Computational Theory". Journal of Neuroscience 16: 3351-3362. 

DeVries, Steven H (December 2000). "Bipolar Cells Use Kainate and AMPA Receptors to Filter Visual Information into Separate Channels". Neuron 28: 847-856. 

Dong, Dawei W (1995). "Temporal Decorrelation: a Theory of Lagged and Nonlagged Responses in the Lateral Geniculate Nucleus". Computation in Neural Systems 6: 159-178. 

Ichida, Jennifer M (2002). "Organization of the Feedback Pathway from Striate Cortex (V1) to the Lateral Geniculate Nucleus (LGN) in the Owl Monkey". Comparative Neurology 454: 272-283. 

Masland, Richard H (1996). "Processing and Encoding of Visual Information in the Retina". Current Oppinion in Neurobiology 6: 467-474. 

Masland, Richard H (2001). "The Fundamental Plan of the Retina". Nature Neuroscience 4 (9). 

Masland, Richard H (23 May 2003). "The Retina's Fancy Tricks". Nature 423: 387-388. 

Masland, Richard H (2004). "Neuronal Cell Types". Current Biology 14: R497-R500. 

Merigan, W H Merigan (1993). "How Parallel are the Primate Visual Pathways?". Annu. Rev. Neurosci. 16: 369-402. 

Nicholls, John G.; A. Robert Martin, Bruce G. Wallace, Paul A. Fuchs (2001). From Neuron to Brain. Boston, Massachusetts: Sinauer Associates, Inc. ISBN 0-87893-439-1. 

Reid, R Clay (2002). "Space and Time Maps of Cone Photoreceptor Signals in Mcaque Lateral Geniculate Nucleus". Journal of Neuroscience 22: 6158-6175. 

Reinagel, Pamela (1999). "Encoding of Visual Information by LGN Bursts". Neurophysiology 81: 2558-2569. 

Srinivasan, M V (1982). "Predictive Coding: a Fresh View of Inhibition in the Retina". Proc. R. Soc. Lond. B216: 427-495.