The intricate involvement of the Insulin-like growth factor receptor signaling in mild traumatic brain injury in mice.

Abstract

Insulin-like growth factor-1 (IGF-1) was suggested as a potential neuroprotective treatment for traumatic brain injury (TBI) induced damage (cognitive as well as cellular). The main goal of the present study was to evaluate the role of the IGF-1R activation in spatial memory outcome following mild traumatic brain injury. mTBI-induced phosphorylation of IGF-1R, AKT and ERK1/2, in mice hippocampus, which was inhibited when mice were pretreated with the selective IGF-1R inhibitor AG1024. IGF-1 administration prevented spatial memory deficits following mTBI. Surprisingly, blocking the IGF-1R signaling in mTBI mice did not augment the spatial memory deficit. In addition, this data imply an intriguing and complex role of the IGF-1 signaling axis in the cellular and behavioral events following mTBI.

• Authors: Vardit Rubovitch, Shahaf Edut, Rive Sarfstein, Haim Werner, Chaim G Pick
• Journal: Neurobiology of disease (Neurobiol Dis) Vol. 38 Issue 2 Pg. 299-303 (May 2010) ISSN: 1095-953X [Electronic] United States
• PMID: 20138993 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright 2010 Elsevier Inc. All rights reserved.

Chemical References

• Insulin-Like Growth Factor I
• Receptor, IGF Type 1
• Proto-Oncogene Proteins c-akt
• Extracellular Signal-Regulated MAP Kinases

Topics

• Animals
• Blotting, Western
• Brain Injuries (metabolism)
• Extracellular Signal-Regulated MAP Kinases (metabolism)
• Hippocampus (drug effects, metabolism)
• Insulin-Like Growth Factor I (metabolism, pharmacology)
• Male
• Mental Recall (drug effects, physiology)
• Mice
• Mice, Inbred ICR
• Phosphorylation (drug effects, physiology)
• Proto-Oncogene Proteins c-akt (metabolism)
• Receptor, IGF Type 1 (metabolism)
• Signal Transduction (drug effects, physiology)
• Spatial Behavior (drug effects, physiology)