Abstract
Unilateral asphyxial neuronal injury was induced in rats by carotid ligation followed by inhalational asphyxia. Infarction and neuronal loss occurs in the ligated hemisphere. In situ hybridisation showed enhanced expression of IGF-I by glia and of its binding proteins BP-2 and BP-3 within 24-72 hours of injury although the distribution of expression showed differences. In contrast IGF-2 and BP-5 were induced much later not appearing for 7-10 days post injury. BP-4 was suppressed on the side of injury. IGF-I was administered to adult rats via the lateral ventricle. Treatment 2 hours after injury led to a dose dependent reduction in infarction from 87% to 26% (p<0.05) over the dose range 5 to 50μg/rat. Functional testing showed protected somatosensory function in the treated rats compared to sham controls. The effect of IGF-1 was not mimicked by des 1-3 IGF-1 suggesting an important role for the induced BP-2 or BP-3. Insulin had a weaker effect than IGF-1 and no protective effect of IGF-2 was observed: compatible with an action at the type 1 IGF receptor. Treatment prior to injury had no effect suggesting that IGF-I acts via interfering with apoptosis. These observations suggest endogenous IGF-1 production is enhanced following neuronal injury as a protective response and suggests that exogenous IGF-1 might be a potential neuronal rescue therapy.
Article PDF
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Gluckman, P., Guan, J., Beilharz, E. et al. A ROLE FOR IGF-1 AND ITS BINDING PROTEINS IN NEURONAL RESCUE FOLLOWING ASPHYXIAL INJURY. Pediatr Res 33 (Suppl 5), S37 (1993). https://doi.org/10.1203/00006450-199305001-00204
Issue Date:
DOI: https://doi.org/10.1203/00006450-199305001-00204