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

doi:10.1016/j.nbd.2010.01.021

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 journal › Article › peer-review

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 language	English
Pages (from-to)	299-303
Number of pages	5
Journal	Neurobiology of Disease
Volume	38
Issue number	2
DOIs	https://doi.org/10.1016/j.nbd.2010.01.021
State	Published - May 2010

Keywords

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

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10.1016/j.nbd.2010.01.021

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title = "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.",

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author = "Vardit Rubovitch and Shahaf Edut and Rive Sarfstein and Haim Werner and Pick, {Chaim G.}",

note = "Funding Information: This work was supported by the Adams Super Center for Brain Studies, Sackler Faculty of Medicine, Tel Aviv University . ",

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AU - Werner, Haim

AU - Pick, Chaim G.

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KW - Y-maze test

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

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Keywords

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