scholarly journals Time-Lapse Retinal Ganglion Cell Dendritic Field Degeneration Imaged in Organotypic Retinal Explant Culture

2016 ◽  
Vol 57 (1) ◽  
pp. 253 ◽  
Author(s):  
Thomas V. Johnson ◽  
Ericka N. Oglesby ◽  
Matthew R. Steinhart ◽  
Elizabeth Cone-Kimball ◽  
Joan Jefferys ◽  
...  
Keyword(s):  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Time Lapse ◽  
Explant Culture ◽  
Retinal Ganglion ◽  
Dendritic Field

scholarly journals Stentian structural plasticity in the developing visual system

2020 ◽  
Vol 117 (20) ◽  
pp. 10636-10638 ◽  
Author(s):  
Tasnia N. Rahman ◽  
Martin Munz ◽  
Elena Kutsarova ◽  
Olesia M. Bilash ◽  
Edward S. Ruthazer
Keyword(s):  
Visual System ◽  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Optic Tectum ◽  
Structural Plasticity ◽  
Time Lapse ◽  
Retinal Ganglion ◽  
Tetanus Neurotoxin ◽  
Contralateral Eye ◽  
Time Lapse Imaging

In a small fraction of Xenopus tadpoles, a single retinal ganglion cell (RGC) axon misprojects to the ipsilateral optic tectum. Presenting flashes of light to the ipsilateral eye causes that ipsilateral axon to fire, whereas stimulating the contralateral eye excites all other RGC inputs to the tectum. We performed time-lapse imaging of individual ipsilaterally projecting axons while stimulating either the ipsilateral or contralateral eye. Stimulating either eye alone reduced axon elaboration by increasing branch loss. New branch additions in the ipsi axon were exclusively increased by contralateral eye stimulation, which was enhanced by expressing tetanus neurotoxin (TeNT) in the ipsilateral axon, to prevent Hebbian stabilization. Together, our results reveal the existence of a non−cell-autonomous “Stentian” signal, engaged by activation of neighboring RGCs, that promotes exploratory axon branching in response to noncorrelated firing.

A suprachiasmatic nucleus projecting retinal ganglion cell exhibits an unusually large dendritic field in the hamster

Neuroreport ◽  
2006 ◽  
Vol 17 (14) ◽  
pp. 1469-1472 ◽  
Author(s):  
Mingliang Pu ◽  
Baiyu Chen ◽  
Rachel S. Li ◽  
David Tay ◽  
Kwok-Fai So
Keyword(s):  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Suprachiasmatic Nucleus ◽  
Retinal Ganglion ◽  
Dendritic Field

Author response for "Identification of Retinal Ganglion Cell Types and Brain Nuclei expressing the transcription factor Brn3c/Pou4f3 using a Cre recombinase knock‐in allele"

2020 ◽  
Author(s):  
Nadia Parmhans ◽  
Anne Drury Fuller ◽  
Eileen Nguyen ◽  
Katherine Chuang ◽  
David Swygart ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Cell Types ◽  
Cre Recombinase ◽  
Author Response ◽  
Retinal Ganglion ◽  
Brain Nuclei

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.

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