scholarly journals Contribution of Individual Retinal Ganglion Cell Responses to Velocity and Acceleration Encoding

2007 ◽  
Vol 98 (4) ◽  
pp. 2285-2296 ◽  
Author(s):  
Andreas Thiel ◽  
Martin Greschner ◽  
Christian W. Eurich ◽  
Josef Ammermüller ◽  
Jutta Kretzberg
Keyword(s):  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Visual Motion ◽  
Retinal Ganglion ◽  
Motion Direction ◽  
Velocity Signal ◽  
Stimulus Velocity ◽  
Firing Rates ◽  
Motion Speed ◽  
Velocity Changes

We investigate the capability of turtle retinal ganglion cell (RGC) ensembles to simultaneously encode multiple aspects of visual motion: speed, direction, and acceleration of moving patterns. Bayesian stimulus reconstruction reveals that the instantaneous firing rates of RGCs contain information about all of these stimulus properties. Stimulus velocity is mainly encoded by steady-state firing rates, whereas acceleration can be reconstructed from transient components in RGC activity induced by abrupt velocity changes. Therefore neurons in higher brain areas may in principle extract information about changing velocity from the instantaneous firing activity of RGCs, without the need to compare responses to present velocities to previous ones. However, reconstruction requires the estimation of a combined acceleration and velocity signal, indicating that RGC ensembles signal both properties simultaneously. In accordance with this conclusion, combined velocity/acceleration sensitivity enhances the similarity of artificial spike trains to experimental data by 50% compared with the case of pure velocity tuning. Decoding of motion direction in addition to speed and acceleration requires direction-sensitive cells, which generate higher firing rates for one of the motion directions and therefore show asymmetric velocity tuning. By dividing the entire ensemble of simultaneously recorded cells into one group of direction-sensitive cells and one group with symmetric tuning, we demonstrate that the population of direction-sensitive cells encodes a combination of motion speed, acceleration, and direction. However, estimation of velocity and acceleration is improved by including the larger group of RGC responses that are sensitive to speed but not to motion direction.

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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