Developmental remodeling of relay cells in the dorsal lateral geniculate nucleus in the absence of retinal input
| dc.contributor.author | El-Danaf, Rana N. | en |
| dc.contributor.author | Krahe, Thomas E. | en |
| dc.contributor.author | Dilger, Emily K. | en |
| dc.contributor.author | Bickford, Martha E. | en |
| dc.contributor.author | Fox, Michael A. | en |
| dc.contributor.author | Guido, William | en |
| dc.date.accessioned | 2018-11-19T18:32:11Z | en |
| dc.date.available | 2018-11-19T18:32:11Z | en |
| dc.date.issued | 2015 | en |
| dc.description.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. | en |
| dc.description.sponsorship | National Institute of Health | en |
| dc.description.sponsorship | NIH:EY012716 | en |
| dc.description.sponsorship | NIH: EY016155 | en |
| dc.description.sponsorship | NIH: EY021222 | en |
| dc.description.version | Published version | en |
| dc.format.mimetype | application/pdf | en |
| dc.identifier.doi | https://doi.org/10.1186/s13064-015-0046-6 | en |
| dc.identifier.issue | 1 | en |
| dc.identifier.uri | http://hdl.handle.net/10919/85899 | en |
| dc.identifier.volume | 10 | en |
| dc.language.iso | en | en |
| dc.publisher | BMC | en |
| dc.rights | Creative Commons Attribution 4.0 International | en |
| dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | en |
| dc.subject | Dorsal lateral geniculate nucleus | en |
| dc.subject | Retinogeniculate pathway | en |
| dc.subject | Relay cells | en |
| dc.subject | Retinal ganglion cells | en |
| dc.subject | Dendritic development | en |
| dc.subject | math5 null | en |
| dc.title | Developmental remodeling of relay cells in the dorsal lateral geniculate nucleus in the absence of retinal input | en |
| dc.title.serial | Neural Development | en |
| dc.type | Article - Refereed | en |
| dc.type.dcmitype | Text | en |
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