Optic nerve transection in monkeys may result in secondary degeneration of retinal ganglion cells.

摘要: PURPOSE Interest in neuroprotection for optic neuropathies is, part, based on the assumption that retinal ganglion cells (RGCs) die, not only as a result of direct (primary) injury, but also indirectly negative effects from neighboring dying RGCs (secondary degeneration). This experiment was designed to test whether secondary RGC degeneration occurs after orbital nerve injury monkeys. METHODS The superior one third side transected eight cynomolgus monkeys (Macaca fascicularis). Twelve weeks partial transection, number bodies and inferior halves retina experimental control eyes diameter axons were compared by detailed histomorphometry. Vitreous obtained amino acid analysis. A sham operation performed three additional RESULTS Transection caused loss 55% +/- 13% with fellow (mean SD, t-test, P < 0.00,001, n = 7). Inferior RGCs, directly injured decreased 22% 10% (P 0.002). 83% 12% 0.0008, 5) whereas, 34% 20% 0.02, 5). Intravitreal levels glutamate other acids nerves different 12 injury. Fundus examination, fluorescein angiography, histologic evaluation confirmed there no vascular compromise tissues transection procedure. CONCLUSIONS suggests primary death due is associated surrounding are injured.