Insulin-like growth factor I partly prevents axon elimination in the neonate rat optic nerve

Abstract

Developmental neuronal death ensues after access of innervating neurons to target-derived neurotrophic factors is restricted. Recent evidence suggests, however, that growth factors such as those of the insulin family modulate neuronal death through autocrine/paracrine mechanisms. In rats, retinal ganglion neurons (RGNs) undergo massive death during early postnatal life. During this same period, the expression of various members of the insulin-like growth factor I (IGF-I) protein family is down regulated. To evaluate whether ocular IGF-I might modulate RGN death, we administered IGF-I in the posterior chamber of the eye of newborn rats. Optic nerve fiber number was estimated in control and IGF-I treated animals at postnatal day 5 when RGN death peaks. Intraocular IGF-I treatment at birth partly prevented optic nerve fiber elimination. Because the axon number in the optic nerve correlates to some extent with the RGN number, these results suggest that IGF-I may modulate RGN death in vivo through local interactions.