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Insulin-like growth factor I partly prevents axon elimination in the neonate rat optic nerve
Gabriel Gutiérrez-Ospina1, Andrea Gutiérrez de la Barrera, Jorge Larriva
1Department of Cell Biology and Physiology, Biomedical Research Institute, National University of México, Mexico D.F., 04510, Mexico. gabo@servidor.unam.mx
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.
Insights
Insulin-like growth factor I (IGF-I) may protect developing retinal ganglion neurons (RGNs) from programmed cell death. Intraocular IGF-I administration in newborn rats reduced RGN death, suggesting a local protective role.
Area of Science:
- Neuroscience
- Developmental Biology
- Endocrinology
Background:
- Developmental neuronal death is a normal process regulated by neurotrophic factors.
- Growth factors, including insulin-like growth factors, may influence neuronal survival via autocrine/paracrine signaling.
- Retinal ganglion neurons (RGNs) in rats experience significant cell death during early postnatal development.
Purpose of the Study:
- To investigate the potential role of ocular Insulin-like Growth Factor I (IGF-I) in modulating RGN death.
- To determine if exogenous IGF-I administration can affect RGN survival in vivo.
Main Methods:
- Newborn rats received intraocular administration of IGF-I in the posterior eye chamber.
- Optic nerve fiber counts were assessed at postnatal day 5, a peak period for RGN death.
- Control groups received no treatment or a placebo.
Main Results:
- Intraocular IGF-I treatment at birth partially inhibited the elimination of optic nerve fibers.
- A correlation exists between optic nerve axon number and RGN survival.
- IGF-I administration demonstrated a protective effect on RGNs.
Conclusions:
- Local ocular IGF-I administration can modulate developmental RGN death in vivo.
- IGF-I may play a crucial role in regulating RGN survival during early postnatal life.
- These findings highlight IGF-I as a potential therapeutic target for conditions involving RGN loss.