Slit1 and Slit2 are present in the ventral diencephalon. Individual mouse knockouts of Slit1 or Slit2 show few RGC axon guidance defects but double mutants develop a large additional chiasm anterior to the true chiasm, and many RGC axons project into the contralateral optic nerve and some extend dorsal or lateral to the chiasm Plump et al.
Similar studies remain to be performed on Robo2 knockout mice Long et al. These data are reminiscent of Slit1; Slit2 double-mutant phenotypes Plump et al.
Anatomy of eye development
A recent study showed that cell surface HS promotes Slit—Robo binding and is important for the repulsive activities of Slit2 protein Hu Moreover, reduction of one allele of EXT1 in Slit2 knockout mutants causes similar axon misguidance at the optic chiasm Inatani et al. These results demonstrate a strong dosage-sensitive genetic interaction between Slit2 and EXT1, indicating that HS plays an essential role in Slit-mediated axon guidance at the optic chiasm. In humans, the optic chiasm lies directly above the diaphragma sallae.
The guidance molecules discussed above may thus affect the precise anatomical location of the human optic chiasm. In the former section, we reviewed recent progress on the mechanism of optic chiasm formation and contralateral crossing over of retinal axons. However, in most mammals, RGC axons derived from the temporal retina avoid the midline and project ipsilaterally Jeffery This arrangement at the level of the optic chiasm is necessary for acquiring high-quality binocular vision and stereopsis.
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Ephrin-B2 and EphB1 control axon divergence at the optic chiasm Williams et al. Ephrin-B2 is expressed in radial glial cells at the optic chiasm concurrent with the development of the ipsilateral projections, and the blockade of ephrin-B2 eliminates the ipsilateral projection in mice.
EphB1; EphB2; EphB3 triple mutants exhibit no more severe phenotype compared with the EphB1 single mutant, indicating an absence of redundancy such that only EphB1 may be up-regulated in growth cones as they enter the chiasm region Williams et al. For example, in Vax2-null mice, ephrin-B2 expression is extended to the ventral retina, but EphB2 is almost absent EphB1 expression was not examined Barbieri et al.
In addition to such a molecular dorsalization of the developing retina see Fig. This phenotype was not reproduced in an independent study Mui et al. Another candidate for regulating ipsilateral projections is the zinc-finger transcription factor Zic2 that is expressed in differentiated VT RGCs when the ipsilateral projection is formed Herrera et al.
In VT RGCs, Zic2 expression is spatiotemporally identical to that of EphB1 and the loss- and gain-of-function analyses indicate that Zic2 is sufficient to switch the outgrowth behavior of retinal axons from crossed to uncrossed patterns in response to inhibitory cues from chiasm cells. In addition, genetic hypomorphs of Zic2 display reduced ipsilateral projection. The phenotype appears similar to that of EphB1 mutants, although these mice also exhibit abnormal RGC axons that project between the optic nerve and chiasm. These findings suggest that Zic2 may control the ipsilateral projection by directly regulating multiple guidance genes including EphB1.
The proportion of Zic2 -expressing cells correlates with the spatiotemporal features of the formation of the uncrossed projection in such diverse species as the mouse, ferret, Xenopus , and chick, and reflects the degree of binocularity in each of these species, implicating Zic2 function in patterning binocular vision throughout evolution Herrera et al. Topographic mapping of RGC axons occurs along two sets of orthogonally oriented axes. In mouse retina, EphA5 and EphA6 are expressed in a decreasing gradient from temporal to nasal axons, while ephrin-A2 and ephrin-A5 from the posterior to the anterior SC Fig.
In ephrin-A2; ephrin-A5 double-mutant mice, both temporal and nasal RGCs exhibit mapping defects, and the ectopic terminations of nasal RGCs are found anterior to their correct P—A sites Feldheim et al. These results support the idea that EphA gradients in the retina and ephrin-A gradients in the SC may operate in combination with axon—axon competition in map formation.
For example, EphA7 shows the strongest anterior-high and posterior-low expression in the SC, but is absent in the retina. A recent study showed that EphA7 is a repellent substrate for retinal axon growth in vitro, and topographic mapping of both temporal and nasal axons is disturbed in EphA7 mutant mice Rashid et al. One recent study reported that an external gradient of Engrailed-2, a homeodomain transcription factor, repels growth cones of Xenopus axons originating from the temporal retina, but attracts nasal axons Brunet et al.
In engrailed-misexpressing chicken tectum, Eph ligand family 1 ELF-1 and repulsive axon guidance signal RAGS that belong to the family of ligands for Eph-related receptor tyrosine kinases are up-regulated Logan et al. In addition, axons from nasal retina frequently arborized at various sites including the inappropriate anterior tectum Itasaki and Nakamura Taken together, Engrailed-2 may also participate in the formation of P—A axis in the vertebrate SC, possibly by regulating the expression of Eph family members Drescher et al.
RGC axons are distributed to specific target zones by responding to gradients of ephrin ligands in SC. Axons from temporal retina, which express high levels of EphA receptors, map to the anterior part in SC blue and black axons while low-EphA-expressing RGCs from nasal retina can invade into the more posterior part red axons. Axons from ventral retina, which express high levels of EphB receptors, map to the medial part in SC blue axons while low-EphB-expressing RGCs from dorsal retina map to the lateral part black and red axons. The phenotype is equivalent or more severe in mice in which the kinase domain and C terminus of EphB2 is replaced with LacZ, indicating that forward signaling dominates over reverse signaling.
These findings imply that EphB-expressing axons are attracted medially by ephrin-B1, in contrast to the repulsive effect of ephrin-B2 at the optic chiasm Williams et al. As mentioned in the former section, in Vax2-null mice the expression of D—V retinal markers is altered, including a reduced expression of EphB2 and EphB3 in ventral retina, and VT RGCs show a complete shift in their target zones from medial to lateral SC Barbieri et al.
Thus, L1 function is likely required for the accurate performance for EphA and EphB mediated positioning. RGC projections from both eyes initially intermingle, but then segregate postnatally and form eye-specific layers in the dLGN. Ephrin-A2 and ephrin-A5 are expressed in ventral—lateral—anterior-high and dorsal—medial—posterior-low gradients, whereas ephrin-A3 is expressed in small amounts in the dLGN. In ephrin-A2; ephrin-A5 double mutants and ephrin-A2; ephrin-A3; ephrin-A5 triple mutants, eye-specific inputs segregate but the shape and location of eye-specific layers are profoundly disrupted Pfeiffenberger et al.
Inhibition of correlated neural activity by a nicotinic acetylcholine receptor antagonist in ephrin-A2; ephrin-A3; ephrin-A5 triple mutants leads to overlapping retinal projections that are located in inappropriate regions of the dLGN, suggesting that regions of the dLGN that are normally occupied by the contralateral eye become competent for innervation from either eye Pfeiffenberger et al. In the mammalian brain, reciprocal connections between sensory nuclei of the dLGN and visual cortical area of the neocortex are essential for the relay and processing of visual information Garel and Rubenstein Recent studies have shown that activity-dependent mechanisms may not be required for the generation of topography of somatosensory and visual cortical maps Crair ; Katz and Crowley These results suggest that activity-independent mechanisms must be required for the generation of topographic maps in the cortex.
During development, TC axons grow into the subcortical telencephalon ST , where postnatally they continue on their paths to the cortex. Recent studies have suggested the requirement of some guidance cues in the ST, which may have a key role in controlling the initial topography of thalamic projections to the neocortex. Ebf1 mutant embryos project dLGN axons abnormally into the amygdalar region or become trapped in the ST. Ebf1 -null TC axons outside the dLGN reach the cerebral cortex but show a global caudal shift in topography Garel et al.
This shift occurs in the absence of an apparent change in thalamic or neocortical reorganization, and is preceded by a shift in the positions of thalamic axons in the ST. The Dlx1 and Dlx2 homeodomain transcription factors are expressed in the ventral thalamus and ST, but are absent from the DT and cortical neurons. In Dlx1; Dlx2 double-mutant embryos, some thalamic axons including axons from the dLGN fail to grow and remain in the ST, and the other axons reach the cortex but exhibit a similar shift in topography, as observed in Ebf1 mutants Garel et al.
On the other hand, EphAs in the thalamus and ephrin-As in the ST are involved in the regulation of TC projections in the somatosensory area in the frontal cortex Dufour et al. These findings suggest that various genes affecting the relative positioning of TC axons within the ST may modify the cortical area, including the visual cortex. Developmental pathfinding of TC axon projections. Ebf1, Dlx1, and Dlx2 expressed in the thalamus and ST affect the relative positioning of TC axons during embryonic development.
Neurotrophins also influence the process of formation of TC connections. Both BDNF and NT-3 are expressed in the cerebral cortex during the critical period when TC axons invade the cortical plate and establish layer-specific synaptic connections with cortical neurons Lein et al. Infusion of BDNF or blockade of TrkB signaling inhibits the formation of ocular dominance columns in the cat visual cortex Cabelli et al. NT-3 is specifically expressed in the layer 4 of the cat visual cortex, both before and during the critical period of TC synapse formation Lein et al. Conditional mutants in which NT-3 is completely deleted in the cerebral cortex result in reduction of TC projections to the visual cortex, and show a phenotype of impaired visual function, which is one of relative cortical blindness Ma et al.
These findings implicate neurotrophins in the critical stage of precise TC projections to the visual cortex Fig. Further studies to reveal the detailed function of neurotrophins during the development of the whole visual pathway may provide important information for the progress of therapeutic methods in RGC protection, regeneration, and rearrangement of TC connections. These experimental molecular and genetic findings begin to provide a comprehensive picture of the intricate interplay between transcription factors and signaling at the cell membrane that leads to the complex and precise wiring achieved by the visual system.
We are grateful to Dr. Dyer for critical review of the manuscript, and Dr. Sakai for his assistance and helpful discussions. We apologize if we have inadvertently omitted pertinent references. View all Molecular regulation of visual system development: more than meets the eye Takayuki Harada 1 , 2 , Chikako Harada 1 , 2 , and Luis F. Previous Section Next Section. Figure 1.
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Demyanenko, G. Drescher, U. You can change your ad preferences anytime. Development Of Vision. Upcoming SlideShare. Like this presentation? Why not share! Embed Size px. Start on. Show related SlideShares at end. WordPress Shortcode. Manoj Aryal , Consultant Optometrist Follow. Full Name Comment goes here.
Are you sure you want to Yes No. Tsietsi Nkhumishe Nkambule. Tari Adrian. It is located on the medial surface of the occipital lobe. The region lies above and below the posterior limb of the calcarine sulcus, and extends anteriorly, below the anterior limb of the calcarine sulcus. The primary visual cortex registers information from the contralateral side. Upper and lower visual fields are crossed. Central vision is represented more posteriorly macula is most posterior , while peripheral vision is represented progressively more anteriorly. The visual association areas are located in Brodmann areas 18 and The superior brachium contains axonal fibers that bypass the thalamus to project to the tectum of the midbrain.
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