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Central administration of insulin-like growth factor-I decreases depressive-like behavior and brain cytokine expression in mice

Overview of attention for article published in Journal of Neuroinflammation, February 2011
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Title
Central administration of insulin-like growth factor-I decreases depressive-like behavior and brain cytokine expression in mice
Published in
Journal of Neuroinflammation, February 2011
DOI 10.1186/1742-2094-8-12
Pubmed ID
Authors

Sook-Eun Park, Robert Dantzer, Keith W Kelley, Robert H McCusker

Abstract

Exogenous administration of insulin-like growth factor (IGF)-I has anti-depressant properties in rodent models of depression. However, nothing is known about the anti-depressant properties of IGF-I during inflammation, nor have mechanisms by which IGF-I alters behavior following activation of the innate immune system been clarified. We hypothesized that central IGF-I would diminish depressive-like behavior on a background of an inflammatory response and that it would do so by inducing expression of the brain-derived neurotrophic factor (BDNF) while decreasing pro-inflammatory cytokine expression in the brain. IGF-I (1,000 ng) was administered intracerebroventricularly (i.c.v.) to CD-1 mice. Mice were subsequently given lipopolysaccharide i.c.v. (LPS, 10 ng). Sickness and depressive-like behaviors were assessed followed by analysis of brain steady state mRNA expression. Central LPS elicited typical transient signs of sickness of mice, including body weight loss, reduced feed intake and decreased social exploration toward a novel juvenile. Similarly, LPS increased time of immobility in the tail suspension test (TST). Pretreatment with IGF-I or antidepressants significantly decreased duration of immobility in the TST in both the absence and presence of LPS. To elucidate the mechanisms underlying the anti-depressant action of IGF-I, we quantified steady-state mRNA expression of inflammatory mediators in whole brain using real-time RT-PCR. LPS increased, whereas IGF-I decreased, expression of inflammatory markers interleukin-1ß (IL-1ß), tumor necrosis factor-(TNF)α, inducible nitric oxide synthase (iNOS) and glial fibrillary acidic protein (GFAP). Moreover, IGF-I increased expression of BDNF. These results indicate that IGF-I down regulates glial activation and induces expression of an endogenous growth factor that shares anti-depressant activity. These actions of IGF-I parallel its ability to diminish depressive-like behavior.

Twitter Demographics

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Mendeley readers

The data shown below were compiled from readership statistics for 127 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United States 5 4%
Chile 1 <1%
Russia 1 <1%
Italy 1 <1%
Croatia 1 <1%
Poland 1 <1%
Unknown 117 92%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 23 18%
Student > Master 23 18%
Researcher 17 13%
Student > Bachelor 12 9%
Student > Doctoral Student 12 9%
Other 22 17%
Unknown 18 14%
Readers by discipline Count As %
Neuroscience 27 21%
Agricultural and Biological Sciences 27 21%
Medicine and Dentistry 17 13%
Psychology 11 9%
Pharmacology, Toxicology and Pharmaceutical Science 7 6%
Other 12 9%
Unknown 26 20%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 22 October 2013.
All research outputs
#3,066,140
of 4,507,509 outputs
Outputs from Journal of Neuroinflammation
#452
of 659 outputs
Outputs of similar age
#68,194
of 101,867 outputs
Outputs of similar age from Journal of Neuroinflammation
#15
of 20 outputs
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