Abstract
Purpose: :
In the DBA/2J mouse model of glaucoma, transport dysfunction is one of the early changes in the pathologyof retinal ganglion cells (RGCs). It is unclear how this deficit relates to dendritic abnormalities that have been reported in this model. Here we examined the morphology of differentially transporting RGCs in DBA/2J mice of various ages.
Methods: :
To label differentially transporting RGCs, cholera toxin subunit B (CTB) was injected intravitreally. One to three days after injection, the retina was dissected and placed in oxygenated Ames medium. Lucifer Yellow or Alexa Fluor 568 was then injected into the soma of differentially transporting RGCs via glass micropipette electrodes.
Results: :
As expected, 3 month old animals had very few RGCs lacking uptake of CTB; most of the cells had normal appearing dendritic morphology. Occasionally an RGC was found that had lost higher order dendritic branching. In contrast, for 10 month old animals, RGC uptake and transport was severely compromised. Many cellshad some degree of dendrite abnormalities ranging from loss of higher order branching with retention of first and second order arborizations to loss of all branching beyond the proximal primary processes. This was so regardless of CTB uptake and axonal transport.n most cases these neurons exhibited normal axons. Occasionally contorted axons were evident.
Conclusions: :
In young DBA/2J mice dendritic morphology appeared normal along with uptake and transport. In aged mice dendritic pruning was widespread but highly variable and unrelated to CTB uptake and transport, which often persisted after pruning.Thus, dendrite loss is an early injury in the DBA/2J mouse that may precede compromised uptake and transport.
Keywords: ganglion cells • degenerations/dystrophies • retinal degenerations: cell biology