GM1 reduces injury-induced metabolic deficits and degeneration in the rat optic nerve.
This study demonstrates the earliest reported effects of GM1 treatment on crush-injured axons of the mammalian optic nerve. GM1, administered intraperitoneally immediately after injury, was found to reduce the injury-induced metabolic deficit in nerve activity within 2 hr of injury, as measured by changes in the nicotine-amine adenine dinucleotide redox state. After 4 wk, transmission electron microscopy 1 mm distal to the site of injury revealed a sevenfold increase in axonal survival in GM1-treated compared to untreated injured nerves. These results emphasize the beneficial effect of GM1 on injured optic nerves as well as the correlation between immediate and long-term consequences of the injury. Thus, these results have implications for treating damaged optic nerves.
Yoles
E
E
Department of Neurobiology, Weizmann Institute of Science, Rehovot, Israel.
Zalish
M
M
Lavie
V
V
Duvdevani
R
R
Ben-Bassat
S
S
Schwartz
M
M
D000818:Animals; D001369:Axons / Q000378:metabolism; D002452:Cell Count; D002470:Cell Survival; D004195:Disease Models, Animal; D005677:G(M1) Ganglioside / Q000494:pharmacology*; D007274:Injections, Intraperitoneal; D008297:Male; D009243:NAD / Q000378:metabolism*; D009410:Nerve Degeneration / Q000187:drug effects*; D009900:Optic Nerve / Q000378:metabolism* / Q000648:ultrastructure; D020221:Optic Nerve Injuries; D051381:Rats; D017207:Rats, Sprague-Dawley; D013050:Spectrometry, Fluorescence
D009243:NAD; D005677:G(M1) Ganglioside