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

Authors

Rana N. El-Danaf, University of California - San Diego
Thomas E. Krahe, Virginia Commonwealth UniversityFollow
Emily K. Dilger, Society for Neuroscience
Martha E. Bickford, University of Louisville
Michael A. Fox, Virginia Polytechnic Institute and State University
William Guido, University of Louisville

Document Type

Article

Original Publication Date

2015

Journal/Book/Conference Title

Biomed Central

Volume

10

Issue

19

DOI of Original Publication

10.1186/s13064-015-0046-6

Comments

Originally published at http://dx.doi.org/10.1186/s13064-015-0046-6

Date of Submission

November 2015

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 themath5 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 frommath5−/− 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.

Rights

Copyright © 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.

Is Part Of

VCU Anatomy and Neurobiology Publications