Idiopathic Bilateral Optic Atrophy in the Rhesus Macaque

Abstract

The existence of BOA in nonhuman primates warrants caution on the part of investigators who use these animals in experimental models of ophthalmic disease.

Cupping in the Monkey Optic Nerve Transection Model Consists of Prelaminar Tissue Thinning in the Absence of Posterior Laminar Deformation

“…14,36 Regarding the evidence for laminar deformation in the existing monkey optic neuropathies, an idiopathic bilateral optic neuropathy that demonstrated nonglaucomatous pallor of the ONH, accompanied by RNFL thinning most predominant within the maculopapular bundle, has been described in nine monkeys of Chinese origin obtained from two different primate centers. 37 However, no in vivo or postmortem histologic assessment of laminar anatomy was performed. Monkey models for unilateral anterior ischemic optic neuropathy, 38,39 ONT, 9–12,40,41 and chronic optic nerve endothelin exposure, 42–45 as well as bilateral optic neuropathy following primary cerebrospinal fluid (CSF) lowering, 26 have been described.…”

The prevalence of microcystic macular changes on optical coherence tomography of the macular region in optic nerve atrophy of non-neuritis origin: a prospective study

“…There have been no studies correlating OCT findings with histology. There are however earlier histological observations that clearly demonstrate retinal vacuoles in the INL of the retina 22 23. Retrograde axonal degeneration was the likely mechanism in the macaque model.…”

Comparing three different modes of electroretinography in experimental glaucoma: diagnostic performance and correlation to structure

“…The three modes selected were mfERG, ff-ERG and PERG because they have each been evaluated extensively and proven effective in clinical studies of human glaucoma [19,21,13,14,22,23,20,24,15] as well as in previous laboratory studies in NHP eyes after retinal ganglion cell or optic nerve injury [34,28], including EG [35–39,17,40,41,29–31]. To our knowledge, however, no prior study has compared all three modes in the same cohort of glaucomatous eyes.…”

“…Specifically, based on previous evidence, we anticipated that the HFC amplitude of the slow-sequence mfERG [17,28–31], the PhNR amplitude of the red-on-blue ff-ERG [36,38,42,43,28] and the N95 of the transient PERG [19,38,34,28] would be the parameters from each mode that would have the strongest diagnostic capacity and correlation to structural damage. These expectations were confirmed by the results, yet the findings also demonstrate that the mfERG HFC amplitude normalized to the mfERG LFC P1 ampltidue had the highest sensitivity and strongest correlation to structural loss.…”