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

Vardit Rubovitch, Shahaf Edut, Rive Sarfstein, Haim Werner, Chaim G. Pick*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

55 Scopus citations

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.

Original languageEnglish
Pages (from-to)299-303
Number of pages5
JournalNeurobiology of Disease
Volume38
Issue number2
DOIs
StatePublished - May 2010

Funding

FundersFunder number
Sackler Faculty of Medicine, Tel Aviv University
Adams Super Center for Brain Studies,Tel Aviv University

    Keywords

    • Akt
    • ERK1/2
    • IGF-1R
    • MTBI
    • Spatial memory
    • Y-maze test

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