Variability in the Location of the Retinal Ganglion Cell Area Centralis Is Correlated with Ontogenetic Changes in Feeding Behavior in the Black Bream, Acanthopagrus butcheri (Sparidae, Teleostei)

2000 ◽  
Vol 55 (4) ◽  
pp. 176-190 ◽  
Author(s):  
Julia Shand ◽  
Stephanie M. Chin ◽  
Alison M. Harman ◽  
Stephen Moore ◽  
Shaun P. Collin
Keyword(s):  
Feeding Behavior ◽  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Cell Area ◽  
Retinal Ganglion ◽  
Ontogenetic Changes ◽  
Black Bream ◽  
Area Centralis ◽  
Acanthopagrus Butcheri

scholarly journals The relationship between the position of the retinal area centralis and feeding behaviour in juvenile black bream Acanthopagrus butcheri (Sparidae: Teleostei)

2000 ◽  
Vol 355 (1401) ◽  
pp. 1183-1186 ◽  
Author(s):  
Julia Shand ◽  
Stephanie M. Chin ◽  
Alison M. Harman ◽  
Shaun P. Collin
Keyword(s):  
Feeding Behaviour ◽  
Ganglion Cell Layer ◽  
High Cell Density ◽  
Cell Layer ◽  
Retinal Ganglion ◽  
High Cell ◽  
Black Bream ◽  
Retinal Ganglion Cell Layer ◽  
Area Centralis ◽  
Acanthopagrus Butcheri

The topography of the neurons in the retinal ganglion cell layer of juvenile black bream Acanthopagrus butcheri changes during development. The region of high cell density, the area centralis (AC), relocates from a temporal (central) to a dorsal (peripheral) position within the dorso-temporal retinal quadrant. Toascertain whether the differences in the position of the AC during development are related to feeding behaviour, we monitored fishes that were given a choice of food. A range of feeding behaviour patterns was recorded in individual fishes. The smallest fishes (8-15mm standard length (SL)) took live food from the water column. Following weaning onto pellets, fishes exhibited a preference for taking food from either the substrate or the surface (but not both).When greater than 20 mm SL, a number of individuals then divided their time between surface and substrate feeding before all fishes became exclusive benthic feeders at a stage between 50 and 80 mm SL. Three individual fishes, for which behaviour patterns were categorized, were killed and the topography of the retinal ganglion cell layer analysed. A range of positions for the AC was found with the smallest fish (12mm SL) possessing a region of high cell density in the temporal retina. In a larger fish (70 mm SL), feeding from both the substrate and the surface, the AC was found in an intermediate dorso-temporal position. The AC of a fish (51mm SL) preferentially taking food from the substrate was located in a dorsal position.

The formation of the area centralis of the retinal ganglion cell layer in the chick

Development ◽  
1987 ◽  
Vol 100 (3) ◽  
pp. 411-420
Author(s):  
C. Straznicky ◽  
M. Chehade
Keyword(s):  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Ganglion Cell Layer ◽  
Cell Layer ◽  
Cell Loss ◽  
Retinal Ganglion ◽  
Retinal Periphery ◽  
Central Retina ◽  
Retinal Ganglion Cell Layer ◽  
Area Centralis

In adult domestic chickens, the neurones in the retinal ganglion cell layer are very unevenly disposed such that there is a sixfold increase in neurone density from the retinal edge to the retinal centre. The formation of the high ganglion-cell-density area centralis was studied on chick retinal wholemounts from the 8th day of incubation (E8) to 4 weeks after hatching (4WAH). The density of viable neurones and the number and the distribution of pyknotic neurones in the ganglion cell layer were estimated across the whole retina. Between E8 and E10, the distribution of neurones in the ganglion cell layer was anisodensitic with 53,000 mm-2 in the centre compared to 34,000 mm-2 in the periphery of the retina. Thereafter, a progressively steeper gradient of neurone density developed, which decreased from 24,000 mm-2 in the retinal centre to 6000 mm-2 at the retinal periphery by 4WAH. Neuronal pyknosis in the ganglion cell layer was observed between E9 and E17. From E11 onwards, consistently more pyknotic neurones were found in the peripheral than in the central retina. It was estimated that over the period of cell death approximately twice as many neurones died per unit area in the retinal periphery than in the centre. Retinal area measurements and estimation of neurone densities in the ganglion cell layer after the period of neurone generation and neurone death indicated differential retinal expansion, with more expansion in the peripheral than in the central retina. These observations allow us to conclude that the formation of the area centralis of the chick retina involves (1) slightly higher cell generation in the retinal centre, (2) higher rate of cell loss in the retinal periphery and (3) differential retinal expansion.

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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