Insulin-like growth factor I partly prevents axon elimination in the neonate rat optic nerve
Por:
Gutiérrez-Ospina G., Gutiérrez de la Barrera A., Larriva J., Giordano M.
Publicada:
1 ene 2002
Resumen:
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. © 2002 Elsevier Science Ireland Ltd. All rights reserved.
Filiaciones:
Gutiérrez-Ospina G.:
Department of Cell Biology and Physiology, Biomedical Research Institute, National University of México, Mexico D.F. 04510, Mexico
Department of Developmental Neurobiology, Center of Neurobiology, National University of México, Juriquilla, Queretaro 76116, Mexico
Gutiérrez de la Barrera A.:
Department of Developmental Neurobiology, Center of Neurobiology, National University of México, Juriquilla, Queretaro 76116, Mexico
Larriva J.:
Department of Developmental Neurobiology, Center of Neurobiology, National University of México, Juriquilla, Queretaro 76116, Mexico
Giordano M.:
Department of Developmental Neurobiology, Center of Neurobiology, National University of México, Juriquilla, Queretaro 76116, Mexico
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