Anterior ischemic optic neuropathy is the most common cause of persist
ent monocular visual loss in persons over the age of 50. At the heart
of this form of optic neuropathy is a sequence of cytoplasmic and memb
rane events that culminate in axonal destruction. Early depletion of A
TP is followed by membrane depolarization, influx of Na+ and Ca2+ via
specific voltage-gated channels and reverse operation of the Na+/Ca2exchange protein. Toxic Ca2+ overload is the ultimate consequence of t
hese events. Preventing or modulating any of these well-defined steps
mitigates against the development of anoxic injury. Translating these
molecular insights about how optic nerve axons are damaged by ischemia
-like conditions into clinical gains remains the challenge for the fut
ure. (C) 1997 Wiley-Liss, Inc.