Antibodies to gangliosides inhibit goldfish optic nerve regeneration in vivo
Intraocular injection of antiserum to mixed ganglioside or to GM1 inhibited the regeneration of goldfish optic axons following an optic nerve crush. For example, injections of antiserum on 5 consecutive days beginning the day before the crush resulted in a decrease of about 40% in the axonal outgrowth distance measured at 10 days after the crush. The inhibition was observed even when the treatment was begun a few days after the lesion, and greater degrees of inhibition were observed when the treatment was given later in regeneration. This indicates that the antiganglioside serum interfered with axonal elongation more than with the initial sprout formation. The antiganglioside treatment did not impair the enlargement of the cell bodies and nucleoli that accompanies regeneration, nor did it affect fast axonal transport of protein, glycoprotein, or glycolipid in regenerating nerves. Thus inhibition of outgrowth by antiganglioside treatment was not mediated by a gross change in the metabolism of the regenerating neurons. Treatment of normal neurons with the antiserum produced a 20-30% increase in the amount of 3H-glucosamine-labeled glycoproteins and glycolipids conveyed by fast axonal transport. These results suggest that membrane gangliosides may normally influence the supply of axonally transported glycosylated macromolecules. However, the effect of antiganglioside on axonal transport of glycosylated molecules and on axonal outgrowth are not necessarily related to each other.