| Literature DB >> 26497792 |
Jessica Agostinone1, Adriana Di Polo2.
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.Entities:
Keywords: Axonal injury; Dendrite; Glaucoma; Ocular hypertension; Retinal ganglion cell; Synapse
Mesh:
Year: 2015 PMID: 26497792 DOI: 10.1016/bs.pbr.2015.04.012
Source DB: PubMed Journal: Prog Brain Res ISSN: 0079-6123 Impact factor: 2.453