Ocular dominance column
Ocular dominance columns are
orientation columns
.
Ocular dominance columns were important in early studies of
cortical plasticity, as it was found that monocular deprivation causes the columns to degrade, with the non-deprived eye assuming control of more of the cortical cells.[3]
It is believed that ocular dominance columns must be important in
squirrel monkeys either lack or partially lack ocular dominance columns, which would not be expected if they are useful. This has led some to question whether they serve a purpose, or are just a byproduct of development.[4]
History
Discovery
Ocular dominance columns were discovered in the 1960s by
Nobel prize winning work on the structure of the visual cortex in cats. Ocular dominance columns have since been found in many animals, such as ferrets, macaques, and humans.[2] Notably, they are also absent in many animals with binocular vision, such as rats.[5]
Structure
Ocular dominance
macaques all have fairly well defined columns, while squirrel monkeys have quite variable columns. There is even variation in expression in individuals of the same species and in different parts of the cortex of the same individual.[4][7]
The columns are cortical layer 4 and have mostly reciprocal projections to many other parts of the visual cortex.[8]
Relation to other features of V1
The ocular dominance
cytochrome oxidase. These are called cytochrome oxidase "blobs
" because of their scattered blob-like appearance.
All three types of
column are present in the visual cortex of humans[4] and macaques,[6] among other animals. In macaques, it was found that both blobs and pinwheel centers tend to lie in the center of ocular dominance columns,[6] but no particular relation has been found between pinwheel centers and blobs.[6] In humans, the layout of the columns is similar; however, humans have somewhat variable column expression with at least one subject having disordered columns similar to those commonly found in squirrel monkeys.[7]
Most early
squirrel monkeys don't always express columns, and even when they do the cytochrome oxidase blobs are not in register with the ocular dominance columns.[9]
Development
Formation
There is no
spontaneous waves of activity in the retina occur before birth and that these waves are crucial for eye specific segregation of inputs to the LGN by correlating the activity of nearby neurons.[11] Similarly, the correlated activation for the retinal waves may direct development of the ocular dominance columns, which receive input from the LGN.[12] Similar spontaneous activity in the cortex may also play a role.[12][13] In any case, it has been shown that disrupting the retinal waves at least alters the pattern of ocular dominance columns.[12]
Plasticity
Sensitive periods
Although the ocular dominance
activity dependent plasticity. This plasticity is so strong that if the signals from both eyes are blocked the ocular dominance columns will completely desegregate.[14] Similarly, if one eye is closed ("monocular deprivation"),[3] removed[15]("enucleation"), or silenced[16]
during the sensitive period, the size of the columns corresponding to the removed eye shrink dramatically.
Models
Many models have been proposed to explain the development and
Hebbian activity dependent mechanism.[12] Generally, chemotaxis models assume activity independent formation via the action of axon guidance molecules, with the structures only later being refined by activity, but there are now known to be activity dependent [17][18] and activity modifying [19][20]
guidance molecules.
Modified Hebbian learning
One major model of the formation of the stripes seen in ocular dominance
Hebbian competition between axon terminals.[21]
The ocular dominance columns look like long term potentiation and depression, synaptic normalization,[23] neurotrophin release,[24] reuptake,[25] and spike-timing-dependent plasticity.[26]
Chemotaxis
ipsilateral, which would be much easier to explain with activity dependent mechanisms.[28] Despite this, a molecular label that directs the formation of the ocular dominance columns has never been found.[12]
Function
It has long been believed that ocular dominance columns play some role in binocular vision.[12] Another candidate function for ocular dominance columns (and for columns in general) is the minimization of connection lengths and processing time, which could be evolutionarily important.[29] It has even been suggested that the ocular dominance columns serve no function.[4]
Notes
- ^ This means, for example, that neurons in the areas marked in red fire more when a vertical edge is visible, green when a horizontal edge is visible, orange when 45°, etc.
- contralateral column just like the occasional Portuguese speaker may be found in China. It was once believed the columns were discrete units with sharp borders but the idea of fuzzy, mostly continuous regions is now preferred.
- ^ The axon terminals don't actually move, but they grow in size and number according to level of activity, the net result being that the output from any particular neuron moves as it loses connection to one neuron and gains connection to another.
- ^ Toward or near the nose
- ^ Toward or near the temple
- ^ Having no optic chiasm
See also
- Visual cortex
- Ocular dominance
- Orientation columns
- Amblyopia
References
- S2CID 23113015.
- ^ PMID 20053913.
- ^ PMID 702379.
- ^ PMID 15937015.
- PMID 8929431.
- ^ PMID 1465416.
- ^ PMID 17898211.
- PMID 1734518.
- S2CID 8394582.
- PMID 11082053.
- PMID 11832224.
- ^ PMID 18558864.
- PMID 12354401.
- PMID 3746403.
- S2CID 19011361.
- S2CID 3195164.
- PMID 15339650.
- S2CID 6049266.
- S2CID 40393852.
- PMID 15814792.
- ^ PMID 2762813.
- PMID 20720116.
- PMID 8816700.
- PMID 9275231.
- S2CID 23654727.
- S2CID 5264124.
- PMID 11135259.
- S2CID 14400423.
- .
Further reading
- Carreira-Perpinan, M; Lister, R; Goodhill, G (2005). "A computational model for the development of multiple maps in primary visual cortex". Cerebral Cortex. 15 (8): 1222–1233. PMID 15616135.