Citation

Santi A, Genis L, Torres Aleman I. Cereb. Cortex 2018; 28(6): 2007-2014.

Affiliation

Ciberned, C/ Valderrebollo 5, 28031 Madrid, Spain.

Copyright

(Copyright © 2018, Oxford University Press)

DOI

10.1093/cercor/bhx106

PMID

28449086

Abstract

In response to injury, the brain produces different neuroprotective molecules, such as insulin-like growth factor I (IGF-I). However, IGF-I is also taken up by the brain from the circulation in response to physiological stimuli. Herein, we analyzed in mice the relative contribution of circulating and locally produced IGF-I to increased brain IGF-I levels after insult. Traumatic brain injury (TBI) induced by a controlled impact resulted in increased IGF-I levels in the vicinity of the lesion, but mice with low serum IGF-I showed significantly lower increases. Indeed, in normal mice, peripheral IGF-I accumulated at the lesion site after injury, and at the same time serum IGF-I levels decreased. Collectively, these data suggest that serum IGF-I enter into the brain after TBI and contributes to increased brain IGF-I levels at the injury site. This connection between central and circulating IGF-I provides an amenable route for treatment, as subcutaneous administration of IGF-I to TBI mice led to functional recovery. These latter results add further support to the use of systemic IGF-I or its mimetics for treatment of brain injuries.

© The Author 2017. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.

Language: en

Keywords

insulin-like growth factor I; sensorimotor function; traumatic brain injury; treatment of brain injury