The directed growth of retinal axons towards surgically transposed tecta in Xenopus; an examination of homing behaviour by retinal ganglion cell axons

Development ◽  
1990 ◽  
Vol 108 (1) ◽  
pp. 147-158
Author(s):  
J.S. Taylor
Keyword(s):  
Ganglion Cell ◽  
Axon Guidance ◽  
Retinal Ganglion Cell ◽  
Optic Tract ◽  
Retinal Ganglion ◽  
Retinal Axons ◽  
Dorsal Neural Tube ◽  
Abnormal Structure ◽  
Optic Axons ◽  
The Brain

The growth of optic axons towards experimentally rotated tecta has been studied. In stage 24/25 embryos, a piece of the dorsal neural tube, containing the dorsal midbrain rudiment, was rotated through 180 degrees. At later stages of development, the pathways of growing optic axons were investigated by labelling with either horseradish peroxidase or fluorescent dye. It is shown that retinal ganglion cell axons followed well-defined pathways, in spite of the abnormal structure of the brain, and were able to locate displaced tecta. This directed outgrowth of retinal axons in the optic tracts appears to be related either to the tectum or to some other component included in the graft operations. In tadpoles in which the midbrain rudiment was removed, optic axons still followed the normal course of the optic tract. This observation argues against long-range target attraction as being essential in guiding growing retinal axons towards the tectum. An alternative axon guidance mechanism, selective fasciculation, is discussed as a possible alternative to explain the directed axon outgrowth which occurs in both the normal and in these experimentally manipulated tadpoles.

The metalloproteinase ADAM10 is required for retinal ganglion cell axon guidance in the developing visual systems

2007 ◽  
Vol 30 (4) ◽  
pp. 77
Author(s):  
Y. Y. Chen ◽  
C. L. Hehr ◽  
K. Atkinson-Leadbeater ◽  
J. C. Hocking ◽  
S. McFarlane
Keyword(s):  
Ganglion Cell ◽  
Axon Guidance ◽  
Retinal Ganglion Cell ◽  
Growth Cone ◽  
Expression Patterns ◽  
Optic Tract ◽  
Axon Growth ◽  
Proteolytic Processing ◽  
Retinal Ganglion

Background: The growth cone interprets cues in its environment in order to reach its target. We want to identify molecules that regulate growth cone behaviour in the developing embryo. We investigated the role of A disintegrin and metalloproteinase 10 (ADAM10) in axon guidance in the developing visual system of African frog, Xenopus laevis. Methods: We first examined the expression patterns of adam10 mRNA by in situ hybridization. We then exposed the developing optic tract to an ADAM10 inhibitor, GI254023X, in vivo. Lastly, we inhibited ADAM10 function in diencephalic neuroepithelial cells (through which retinal ganglion cell (RGC) axons extend) or RGCs by electroporating or transfecting an ADAM10 dominant negative (dn-adam10). Results: We show that adam10 mRNA is expressed in the dorsal neuroepithelium over the time RGC axons extend towards their target, the optic tectum. Second, pharmacological inhibition of ADAM10 in an in vivo exposed brain preparation causes the failure of RGC axons to recognize their target at low concentrations (0.5, 1 μM), and the failure of the axons to make a caudal turn in the mid-diencephalon at higher concentration (5 μM). Thus, ADAM10 function is required for RGC axon guidance at two key guidance decisions. Finally, molecular inhibition of ADAM10 function by electroporating dn-adam10 in the brain neuroepithelium causes defects in RGC axon target recognition (57%) and/or defects in caudal turn (12%), as seen with the pharmacological inhibitor. In contrast, molecular inhibition of ADAM10 within the RGC axons has no effect. Conclusions: These data argue strongly that ADAM10 acts cell non-autonomously within the neuroepithelium to regulate the guidance of RGC axons. This study shows for the first time that a metalloproteinase acts in a cell non-autonomous fashion to direct vertebrate axon growth. It will provide important insights into candidate molecules that could be used to reform nerve connections if destroyed because of injury or disease. References Hattori M, Osterfield M, Flanagan JG. Regulated cleavage of a contact-mediated axon repellent. Science 2000; 289(5483):1360-5. Janes PW, Saha N, Barton WA, Kolev MV, Wimmer-Kleikamp SH, Nievergall E, Blobel CP, Himanen JP, Lackmann M, Nikolov DB. Adam meets Eph: an ADAM substrate recognition module acts as a molecular switch for ephrin cleavage in trans. Cell 2005; 123(2):291-304. Pan D, Rubin GM. Kuzbanian controls proteolytic processing of Notch and mediates lateral inhibition during Drosophila and vertebrate neurogenesis. Cell 1997; 90(2):271-80.

Effect of polysialic acid on the behavior of retinal ganglion cell axons during growth into the optic tract and tectum

Development ◽  
1995 ◽  
Vol 121 (10) ◽  
pp. 3439-3446 ◽  
Author(s):  
X. Yin ◽  
M. Watanabe ◽  
U. Rutishauser
Keyword(s):  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Polysialic Acid ◽  
Optic Tract ◽  
Retinal Ganglion ◽  
Guidance Cues ◽  
Neural Cell Adhesion ◽  
The Central Nervous System ◽  
Optic Axons ◽  
Free Environment

We have demonstrated previously that the polysialic acid (PSA) moiety of the neural cell adhesion molecule (NCAM) can regulate peripheral nerve branching during development. In particular, it was found that specific enzymatic removal of PSA from motor axons causes them to form tight fascicles that are less responsive to normal guidance cues. In the present study, the role of PSA in the behavior of axons in the central nervous system has been examined through an analysis of chick optic axons during development. Unlike peripheral axons, which generally grow in a PSA-free environment, PSA was found to be present both on retinal ganglion cell axons and their environment in the tract and tectum. Furthermore, the enzymatic removal of PSA from the optic axons caused them to defasciculate in the tract/tectal region. This response was morphologically similar to targeting corrections made by these axons at a later stage when PSA levels have decreased, suggesting that the PSA may serve to shield them from responding prematurely to some guidance cues in their target region.

A developmental and ultrastructural study of the optic chiasma in Xenopus

Development ◽  
1988 ◽  
Vol 102 (3) ◽  
pp. 537-553
Author(s):  
M.A. Wilson ◽  
J.S. Taylor ◽  
R.M. Gaze
Keyword(s):  
Optic Nerve ◽  
Cell Mass ◽  
Light And Electron Microscopy ◽  
Optic Tract ◽  
Retinal Ganglion ◽  
Intercellular Spaces ◽  
Optic Chiasma ◽  
Cell Processes ◽  
Optic Axons ◽  
The Brain

The structure of the optic chiasma in Xenopus tadpoles has been investigated by light and electron microscopy. Where the optic nerve approaches the chiasma, a tongue of cells protrudes from the periventricular cell mass into the dorsal part of the nerve. Glial processes from this tongue of cells ensheath fascicles of optic axons as they enter the brain. Coincident with this partitioning, the annular arrangement of axons in the optic nerve changes to the laminar organization of the optic tract. Beyond the site of this rearrangement, all newly growing axons accumulate in the ventral-most part of the nerve and pass into the region between the periventricular cells and pia which we have called the ‘bridge’. This region is characterized by a loose meshwork of glial cell processes, intercellular spaces and the presence of both optic and nonoptic axons. In the bridge, putative growth cones of retinal ganglion cell axons are found in the intercellular spaces in contact with both the glia and with other axons. The newly growing axons from each eye cross in the bridge at the midline and pass into the superficial layers of the contralateral optic tracts. As the system continues to grow, previous generations of axon, which initially crossed in the existing bridge, are displaced dorsally and caudally, forming the deeper layers of the chiasma. At their point of crossing in the deeper layers, these fascicles of axons from each eye interweave in an intimate fashion. There is no glial segregation of the older axons as they interweave within the chiasma.

Retinal Ganglion Cell Axon Wiring Establishing the Binocular Circuit

2020 ◽  
Vol 6 (1) ◽  
pp. 215-236
Author(s):  
Carol Mason ◽  
Nefeli Slavi
Keyword(s):  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Molecular Mechanisms ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Optic Tract ◽  
Optic Chiasm ◽  
Retinal Ganglion ◽  
Temporal Features ◽  
Ipsilateral Projection

Binocular vision depends on retinal ganglion cell (RGC) axon projection either to the same side or to the opposite side of the brain. In this article, we review the molecular mechanisms for decussation of RGC axons, with a focus on axon guidance signaling at the optic chiasm and ipsi- and contralateral axon organization in the optic tract prior to and during targeting. The spatial and temporal features of RGC neurogenesis that give rise to ipsilateral and contralateral identity are described. The albino visual system is highlighted as an apt comparative model for understanding RGC decussation, as albinos have a reduced ipsilateral projection and altered RGC neurogenesis associated with perturbed melanogenesis in the retinal pigment epithelium. Understanding the steps for RGC specification into ipsi- and contralateral subtypes will facilitate differentiation of stem cells into RGCs with proper navigational abilities for effective axon regeneration and correct targeting of higher-order visual centers.

scholarly journals Retinal ganglion cell defects cause decision shifts in visually evoked defense responses

2020 ◽  
Vol 124 (5) ◽  
pp. 1530-1549
Author(s):  
Rebecca Nicole Lees ◽  
Armaan Fazal Akbar ◽  
Tudor Constantin Badea
Keyword(s):  
Ganglion Cell ◽  
Brain Stem ◽  
Retinal Ganglion Cell ◽  
Genetically Modified ◽  
Visual Stimuli ◽  
Defense Responses ◽  
Retinal Ganglion ◽  
Freezing Response ◽  
Response Choices ◽  
The Brain

Flight and freezing response choices evoked by visual stimuli are controlled by brain stem and thalamic circuits. Genetically modified mice with loss of specific retinal ganglion cell (RGC) subpopulations have altered flight versus freezing choices in response to some but not other visual stimuli. This finding suggests that “threatening” visual stimuli may be computed already at the level of the retina and communicated via dedicated pathways (RGCs) to the brain.

The early development of the frog retinotectal projection

Development ◽  
1991 ◽  
Vol 113 (Supplement_2) ◽  
pp. 95-104
Author(s):  
Jeremy S. H. Taylor
Keyword(s):  
Ganglion Cell ◽  
Early Development ◽  
Short Distance ◽  
Lateral Wall ◽  
Retinal Ganglion ◽  
Initial Development ◽  
Retinal Axons ◽  
A Chain ◽  
The Brain ◽  
Rostral Part

The guidance of retinal ganglion cell axons has been investigated in embryos of the frog Xenopus. During the initial development of the brain a series of axon tracts are laid down forming a basic ‘scaffold’ or framework. Retinal axons grow through one of these tracts, the tract of the post-optic commissure (tPOC). This is the only tract that extends through the rostral part of the brain at these early stages of development. The origin and development of the tPOC has been studied using antibodies which label neurons at their earliest stages of differentiation. The first sign of the tPOC is a chain of neurons which differentiate simultaneously in the caudolateral part of the diencephalon. Axons from these neurons grow the short distance between adjacent cells interlinking the chain to form a descending tract. A series of other axon projections are then added to the tPOC, each of which is segregated into a particular subregion of the tract. Retinal axons are added to the tract approximately 18 h after its formation. They grow in the sub-pial part of the tract and always occupy the rostralmost edge. Retinal axons follow the tract to the region of the developing tectum where they leave, turn dorsally, and terminate. The reliance of retinal axons on this pre-existing pathway has been demonstrated by experimentally altering the course of the tPOC during its early development. The caudo-lateral wall of the diencephalon has been rotated through 90° at a stage just before the tPOC neurons differentiate. Confirmation of the predicted alteration in the course of the tPOC has been made using immunocytochemistry. In such manipulated brains, retinal axons maintain their strong affinity for the rostral edge of the tPOC, following its altered course through the diencephalon.

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