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

Abstract

BackgroundThe 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.ResultsThe 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.ConclusionsRetinal 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.

The Fuzzy Logic of Network Connectivity in Mouse Visual Thalamus

“…A subset of these TCs was innervated by unusually large boutons which, similar to a type that was previously described (Rafols and Valverde 1973; Spacek and Lieberman, 1974, El-Danaf et al, 2015), were perforated by multiple dendritic excrescences (TC spines)(Figures 3E and 7A). These spines sometimes branched and occasionally passed all the way through the bouton.…”

An evolving view of retinogeniculate transmission

“…Simple contacts dominate retinal input onto cat Y cells, whereas X cell dendritic appendages preferentially participate in complex synaptic structures (Robson & Mason, 1979; Hamos et al, 1985; Koch, 1985; Sherman & Guillery, 1996; Sherman, 2004). Similar distinctions among TC neurons have been observed in the mice by morphological analysis, but have not been associated with distinct patterns of synaptic structures nor delineated by physiology (Krahe et al, 2011; El-Danaf et al, 2015; Sriram et al, 2016). …”

Adaptive reorganization of retinogeniculate axon terminals in dorsal lateral geniculate nucleus following experimental mild traumatic brain injury

“…Examination of VGLUT2 immunoreactivity within dLGN allowed for identification of the retinogeniculate axon terminals downstream of the injured optic nerve. Assessment of this immunoreactivity in our sham-injured animals was consistent with previous reports of normal VGLUT2 immunoreactivity by others (El-Danaf et al, 2015; Hammer et al, 2015, 2014). Within sham animals, the distribution of VGLUT2 immunoreactivity occurred in large clusters of variable size, likely composed of multiple axon terminals as they synapse on proximal dendrites of relay neurons.…”

“…Using with two independent methods to identify the downstream axon terminal fields of injured axons and by evaluating both the deafferentation and reorganization response among axon terminals in dLGN, we provide for the first time, insight into the potential consequences of mTBI induced DAI. One of the three vesicular glutamate transporters expressed in mammalian central nervous system, VGLUT2, is necessary for glutamatergic transmission in the diencephalon where dLGN forms and develops and is the specific isoform of VGLUT present in retinogeniculate axon terminals (El-Danaf et al, 2015; Hammer et al, 2015; Moechars et al, 2006). In this regard, VGLUT2 immunohistochemistry provided us with a highly specific method to identify and compare retinogeniculate axon terminals in dLGN across each time point.…”