Retinal ganglion cell dendrite pathology and synapse loss

Abstract

Dendrites are exquisitely specialized cellular compartments that critically influence how neurons collect and process information. Retinal ganglion cell (RGC) dendrites receive synaptic inputs from bipolar and amacrine cells, thus allowing cell-to-cell communication and flow of visual information. In glaucoma, damage to RGC axons results in progressive neurodegeneration and vision loss. Recent data indicate that axonal injury triggers rapid structural alterations in RGC dendritic arbors, prior to manifest axonal loss, which lead to synaptic rearrangements and functional deficits. Here, we provide an update on recent work addressing the role of RGC dendritic degeneration in models of acute and chronic optic nerve damage as well as novel mechanisms that regulate RGC dendrite stability. A better understanding of how defects in RGC dendrites contribute to neurodegeneration in glaucoma might provide new insights into disease onset and progression, while informing the development of novel therapies to prevent vision loss.