The uniqueness of the message in a retinal ganglion cell spike train and its implication for retinal prostheses

2012 ◽  
Author(s):  
J. B. Troy ◽  
F. M. Yrazu ◽  
C. L. Passaglia
Keyword(s):  
Ganglion Cell ◽  
Spike Train ◽  
Retinal Ganglion Cell ◽  
Retinal Ganglion ◽  
Retinal Prostheses

Contrast Adaptation Decreases Complexity in Retinal Ganglion Cell Spike Train

2007 ◽  
Vol 24 (1) ◽  
pp. 271-274 ◽  
Author(s):  
Wang Guang-Li ◽  
Huang Shi-Yong ◽  
Zhang Ying-Ying ◽  
Liang Pei-Ji
Keyword(s):  
Ganglion Cell ◽  
Spike Train ◽  
Retinal Ganglion Cell ◽  
Retinal Ganglion ◽  
Contrast Adaptation

scholarly journals Quantal Encoding of Information in a Retinal Ganglion Cell

2005 ◽  
Vol 94 (2) ◽  
pp. 1048-1056 ◽  
Author(s):  
Michael A. Freed
Keyword(s):  
White Noise ◽  
Ganglion Cell ◽  
Spike Train ◽  
Retinal Ganglion Cell ◽  
Spike Timing ◽  
Retinal Ganglion ◽  
Noise Stimulus ◽  
Excitatory Postsynaptic Currents ◽  
Temporal Precision ◽  
Postsynaptic Currents

A retinal ganglion cell receives information about a white-noise stimulus as a flickering pattern of glutamate quanta. The ganglion cell reencodes this information as brief bursts of one to six spikes separated by quiescent periods. When the stimulus is repeated, the number of spikes in a burst is highly reproducible (variance < mean) and spike timing is precise to within 10 ms, leading to an estimate that each spike encodes about 2 bits. To understand how the ganglion cell reencodes information, we studied the quantal patterns by repeating a white-noise stimulus and recording excitatory currents from a voltage-clamped, brisk-sustained ganglion cell. Quanta occurred in synchronous bursts of 3 to 65; the resulting postsynaptic currents summed to form excitatory postsynaptic currents (EPSCs). The number of quanta in an EPSC was only moderately reproducible (variance = mean), quantal timing was precise to within 14 ms, and each quantum encoded 0.1–0.4 bit. In conclusion, compared to a spike, a quantum has similar temporal precision, but is less reproducible and encodes less information. Summing multiple quanta into discrete EPSCs improves the reproducibility of the overall quantal pattern and contributes to the reproducibility of the spike train.

Spike train signatures of retinal ganglion cell types

2007 ◽  
Vol 26 (2) ◽  
pp. 367-380 ◽  
Author(s):  
Günther M. Zeck ◽  
Richard H. Masland
Keyword(s):  
Ganglion Cell ◽  
Spike Train ◽  
Retinal Ganglion Cell ◽  
Cell Types ◽  
Retinal Ganglion

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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