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      Developmental remodeling of relay cells in the dorsal lateral geniculate nucleus in the absence of retinal input

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          Abstract

          Background

          The dorsal lateral geniculate nucleus (dLGN) of the mouse has been an important experimental model for understanding thalamic circuit development. The developmental remodeling of retinal projections has been the primary focus, however much less is known about the maturation of their synaptic targets, the relay cells of the dLGN. Here we examined the growth and maturation of relay cells during the first few weeks of life and addressed whether early retinal innervation affects their development. To accomplish this we utilized the math5 null ( math5 −/− ) mouse, a mutant lacking retinal ganglion cells and central projections.

          Results

          The absence of retinogeniculate axon innervation led to an overall shrinkage of dLGN and disrupted the pattern of dendritic growth among developing relay cells. 3-D reconstructions of biocytin filled neurons from math5 −/− mice showed that in the absence of retinal input relay cells undergo a period of exuberant dendritic growth and branching, followed by branch elimination and an overall attenuation in dendritic field size. However, math5 −/− relay cells retained a sufficient degree of complexity and class specificity, as well as their basic membrane properties and spike firing characteristics.

          Conclusions

          Retinal innervation plays an important trophic role in dLGN development. Additional support perhaps arising from non-retinal innervation and signaling is likely to contribute to the stabilization of their dendritic form and function.

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          Most cited references59

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          The role of the thalamus in the flow of information to the cortex.

          The lateral geniculate nucleus is the best understood thalamic relay and serves as a model for all thalamic relays. Only 5-10% of the input to geniculate relay cells derives from the retina, which is the driving input. The rest is modulatory and derives from local inhibitory inputs, descending inputs from layer 6 of the visual cortex, and ascending inputs from the brainstem. These modulatory inputs control many features of retinogeniculate transmission. One such feature is the response mode, burst or tonic, of relay cells, which relates to the attentional demands at the moment. This response mode depends on membrane potential, which is controlled effectively by the modulator inputs. The lateral geniculate nucleus is a first-order relay, because it relays subcortical (i.e. retinal) information to the cortex for the first time. By contrast, the other main thalamic relay of visual information, the pulvinar region, is largely a higher-order relay, since much of it relays information from layer 5 of one cortical area to another. All thalamic relays receive a layer-6 modulatory input from cortex, but higher-order relays in addition receive a layer-5 driver input. Corticocortical processing may involve these corticothalamocortical 're-entry' routes to a far greater extent than previously appreciated. If so, the thalamus sits at an indispensable position for the modulation of messages involved in corticocortical processing.
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            Requirement for math5 in the development of retinal ganglion cells.

            math5 is a murine orthologue of atonal, a bHLH proneural gene essential for the formation of photoreceptors and chordotonal organs in Drosophila. The expression of math5 coincides with the onset of retinal ganglion cell (RGC) differentiation. Targeted deletion of math5 blocks the initial differentiation of 80% of RGCs and results in an increase in differentiated amacrine cells. Furthermore, the absence of math5 abolishes the retinal expression of brn-3b and the formation of virtually all brn-3b-expressing RGCs. These results imply that math5 is a proneural gene essential for RGC differentiation and that math5 acts upstream to activate brn-3b-dependent differentiation processes in RGCs.
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              Developmental remodeling of the retinogeniculate synapse.

              Anatomical rearrangement of retinogeniculate connections contributes to the refinement of synaptic circuits in the developing visual system, but the underlying changes in synaptic function are unclear. Here, we study such changes in mouse brain slices. Each geniculate cell receives a surprisingly large number of retinal inputs (>20) well after eye-specific zones are formed. All but one to three of these inputs are eliminated over a 3-week period spanning eye opening. Remaining inputs are strengthened approximately 50-fold, in part through an increase in quantal size, but primarily through an increase in the number of release sites. Changes in release probability do not contribute significantly. Thus, a redistribution of release sites from many inputs to few inputs at this late developmental stage contributes to the precise receptive fields of thalamic relay neurons.
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                Author and article information

                Contributors
                reldanaf@ucsd.edu
                tekrahe@vcu.edu
                edilger@sfn.org
                mebick01@louisville.edu
                mafox1@vtc.vt.edu
                502-852-6227 , william.guido@louisville.edu
                Journal
                Neural Dev
                Neural Dev
                Neural Development
                BioMed Central (London )
                1749-8104
                15 July 2015
                15 July 2015
                2015
                : 10
                : 19
                Affiliations
                [ ]Departments of Neuroscience, Neurobiology Section in the Division of Biological Sciences, University of California, San Diego, La Jolla, CA 92093 USA
                [ ]Department of Anatomy and Neurobiology, Virginia Commonwealth University Medical Center, Richmond, VA 23298 USA
                [ ]Society for Neuroscience, Washington D.C., 20005 USA
                [ ]Department of Anatomical Sciences and Neurobiology, University of Louisville School of Medicine, Louisville, KY 40292 USA
                [ ]Virginia Tech Carilion Research Institute, Roanoke, VA 24016 USA
                [ ]Department of Biological Sciences, Virginia Tech, Blacksburg, VA 24061 USA
                Article
                46
                10.1186/s13064-015-0046-6
                4502538
                26174426
                189550c4-ad61-4162-9504-19b0b87001d2
                © El-Danaf et al. 2015

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 5 January 2015
                : 1 July 2015
                Categories
                Research Article
                Custom metadata
                © The Author(s) 2015

                Neurosciences
                dorsal lateral geniculate nucleus,retinogeniculate pathway,relay cells,retinal ganglion cells,dendritic development,math5 null

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