Insulin-like growth factor I partly prevents axon elimination in the neonate rat optic nerve.
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.
Gutiérrez-Ospina
Gabriel
G
Department of Cell Biology and Physiology, Biomedical Research Institute, National University of México, Mexico D.F., 04510, Mexico. gabo@servidor.unam.mx
Gutiérrez de la Barrera
Andrea
A
Larriva
Jorge
J
Giordano
Magda
M
D000818:Animals; D000831:Animals, Newborn; D017209:Apoptosis / Q000187:drug effects*; D001369:Axons / Q000187:drug effects*; D007334:Insulin-Like Growth Factor I / Q000494:pharmacology*; D009900:Optic Nerve / Q000187:drug effects* / Q000254:growth & development*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012165:Retinal Ganglion Cells / Q000187:drug effects*
D007334:Insulin-Like Growth Factor I