Retinotopy

Retinotopy (from Greek τόπος (tópos) 'place') is the mapping of visual input from the retina to neurons, particularly those neurons within the visual stream. For clarity, 'retinotopy' can be replaced with 'retinal mapping', and 'retinotopic' with 'retinally mapped'.

Visual field maps (retinotopic maps) are found in many amphibian and mammalian species, though the specific size, number, and spatial arrangement of these maps can differ considerably. Sensory topographies can be found throughout the brain and are critical to the understanding of one's external environment. Moreover, the study of sensory topographies and retinotopy in particular has furthered our understanding of how neurons encode and organize sensory signals.

Retinal mapping of the visual field is maintained through various points of the visual pathway including but not limited to the retina, the dorsal

The discovery of visual field maps in humans can be traced to neurological cases, arising from war injuries, described and analyzed independently by Tatsuji Inouye (a Japanese ophthalmologist) and Gordon Holmes (a British neurologist). They observed correlations between the position of the entry wound and visual field loss (see Fishman, 1997^[6] for an historical review).

Development

Molecular Cues

The "Chemoaffinity Hypothesis" was established by Sperry et al in 1963 in which it is thought that molecular gradients in both presynaptic and postsynaptic partners within the optic tectum organize developing axons into a coarse retinotopic map.^[7] This was established after a series of seminal experiments in fish and amphibians showed that retinal ganglion axons were already retinotopically organized within the optic tract and if severed, would regenerate and project back to retinotopically appropriate locations. Later, it was identified that receptor tyrosine kinases family EphA and a related EphA binding molecule referred to as ephrin-A family are expressed in complementary gradients in both the retina and the tectum.^[8][9][10] More specifically in the mouse, Ephrin A5 is expressed along the rostral-caudal axis of the optic tectum^[11] whereas the EphB family is expressed along the medio-lateral axis.^[12] This bimodal expression suggests a mechanism for the graded mapping of the temporal-nasal axis and the dorsoventral axis of the retina.

Target Space

While molecular cues are thought to guide axons into a coarse retinotopic map, the resolution of this map is thought to be influenced by available target space on postsynaptic partners. In wild type mice, it is thought that competition of target space is important for ensuring continuous retinal mapping, and that if perturbed, this competition may lead to the expansion or compression of the map depending on the available space. If the available space is altered, such as lesioning or ablating half of the retina, the healthy axons will expand their arbors in the tectum to fill the space.^[13] Similarly, if part of the tectum is ablated, the retinal axons will compress the topography to fit within the available tectal space.^[14]

Neural Activity

While neural activity in the retina is not necessary for the development of retinotopy, it seems to be a critical component for the refinement and stabilization of connectivity. Dark reared animals (no external visual cues) develop a normal retinal map in the tectum with no marked changes in receptive field size or laminar organization.^[15][16] While these animals may not have received external visual cues during development, these experiments suggest that spontaneous activity in the retina may be sufficient for retinotopic organization. In the goldfish, no neural activity (no external visual cues, and no spontaneous activity) did not prevent the formation of the retinal map but the final organization showed signs of lower resolution refinement and more dynamic growth (less stable).^[17] Based on Hebbian mechanisms, the thought is that if neurons are sensitive to similar stimuli (similar area of the visual field, similar orientation or direction selectivity) they will likely fire together. This patterned firing will result in stronger connectivity within the retinotopic organization through NMDAR synapse stabilization mechanisms in the post synaptic cells.^[18][19]

Dynamic Growth

Another important factor in the development of retinotopy is the potential for structural plasticity even after neurons are morphologically mature. One interesting hypothesis is that axons and dendrites are continuously extending and retracting their axons and dendrites. Several factors alter this dynamic growth including the Chemoaffinity Hypothesis, the presence of developed synapses, and neural activity. As the nervous system develops and more cells are added, this structural plasticity allows for axons to gradually refine their place within the retinotopy.^[20] This plasticity is not specific to retinal ganglion axons, rather it's been shown that dendritic arbors of tectal neurons and filopodial processes of radial glial cells are also highly dynamic.

Description

In many locations within the brain, adjacent

Areas of the visual cortex are sometimes defined by their retinotopic boundaries, using a criterion that states that each area should contain a complete map of the visual field. However, in practice the application of this criterion is in many cases difficult.^[1] Those visual areas of the brainstem and cortex that perform the first steps of processing the retinal image tend to be organized according to very precise retinotopic maps. The role of retinotopy in other areas, where neurons have large receptive fields, is still being investigated.^[21]

Retinotopy mapping shapes the folding of the

Wikimedia Commons has media related to Retinotopy.

• Biological neural network
• Cortical magnification
• Frontal eye field
• Tonotopy
• Visual space

References