Ischemic injury of optic nerve axons: the nuts and bolts.
Anterior ischemic optic neuropathy is the most common cause of persistent 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 membrane events that culminate in axonal destruction. Early depletion of ATP is followed by membrane depolarization, influx of Na+ and Ca2+ via specific voltage-gated channels and reverse operation of the Na+/Ca2+ exchange protein. Toxic Ca2+ overload is the ultimate consequence of these 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 future.
Fern
R
R
Department of Neurology, University of Washington, Seattle 98195, USA. BOBFERN@U.WASHINGTON.EDU
Ransom
B R
BR
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001369:Axons / Q000502:physiology*; D015220:Calcium Channels / Q000378:metabolism; D009412:Nerve Fibers / Q000502:physiology; D009900:Optic Nerve / Q000098:blood supply / Q000503:physiopathology*; D018917:Optic Neuropathy, Ischemic / Q000503:physiopathology*; D015427:Reperfusion Injury / Q000503:physiopathology*; D015222:Sodium Channels / Q000378:metabolism
D015220:Calcium Channels; D015222:Sodium Channels; D000255:Adenosine Triphosphate