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Series GSE71846 Query DataSets for GSE71846
Status Public on Aug 05, 2016
Title Blast traumatic brain injury induced cognitive deficits are attenuated by pre- or post-injury treatment with the glucagon-like peptide-1 receptor agonist, exendin-4 [Day 3 dataset]
Organism Mus musculus
Experiment type Expression profiling by array
Summary Blast traumatic brain injury (B-TBI) affects military and civilian personnel. Presently there are no approved drugs for blast brain injury. Exendin-4, administered subcutaneously, was evaluated as a pre-treatment (48 hours) and post-injury treatment (2 hours) on neurodegeneration, behaviors and gene expressions in a murine open field model of blast injury. B-TBI induced neurodegeneration, changes in cognition and genes expressions linked to dementia disorders. Exendin-4, administered pre- or post-injury ameliorated B-TBI-induced neurodegeneration at 72 hours, memory deficits from days 7-14 and attenuated genes regulated by blast at day 14 post-injury. The present data suggest shared pathological processes between concussive and B-TBI, with endpoints amenable to beneficial therapeutic manipulation by exendin-4. B-TBI-induced dementia-related gene pathways and cognitive deficits in mice somewhat parallel epidemiological studies of Barnes and co-workers who identified a greater risk in US military veterans who experienced diverse TBIs, for dementia in later life.
Overall design Experimental conditions used to create a blast traumatic brain injury (B-TBI) and the subsequent model characterization have been described in detail previously. In short, male ICR mice (30-40 g) were anaesthetized with a combination of ketamine (100 mg/kg) and xylazine (10 mg/kg). Once fully anaesthetized, the animals were positioned ‘side-on’ to the blast overpressure on an elevated platform in a circle, 7 meters from the source of the detonation generated by the detonation of 500 g of trinitrotoluene (TNT). The maximum overpressure generated by the detonation was 2.5 PSI (17.23 kPa). The following animal treatment groups were utilized: sham operated no blast (Sham); blast traumatic brain injury (B-TBI); Ex-4 as a pre-treatment to the blast injury (Ex-4/B-TBI); Ex-4 as a post-treatment to the blast injury (B-TBI/Ex-4) and Ex-4 but no injury (Ex-4). Hippocampal brain gene expression was examined on day 3 and day 14 (Experiment GSE44625) after the blast traumatic brain injury (B-TBI) or sham procedure. Animals received 3.5 pM/kg/min (21ug/kg/day) Exendin-4 using Alzet micro-osmotic pumps either as a pre-treatment to the blast injury 48 hours before (Ex-4 pre-TBI) or as a post-treatment 2 hours after the blast injury (Ex-4 post-TBI). Animals in a previous data set on Day 14 (GSE44625) were administered Ex-4 as a pre-treatment.
Contributor(s) Tweedie D, Rachmany L, Rubovitch V, Li Y, Holloway HW, Lehrmann E, Zhang Y, Becker KG, Perez E, Hoffer BJ, Pick CG, Greig NH
Citation(s) 26327236, 26868732
Submission date Aug 07, 2015
Last update date Jun 22, 2020
Contact name Supriyo De
Organization name NIA-IRP, NIH
Department Laboratory of Genetics and Genomics
Lab Computational Biology & Genomics Core
Street address 251 Bayview Blvd
City Baltimore
State/province Maryland
ZIP/Postal code 21224
Country USA
Platforms (1)
GPL6885 Illumina MouseRef-8 v2.0 expression beadchip
Samples (24)
GSM1846743 Control_replicate 1
GSM1846744 Control_replicate 2
GSM1846745 Control_replicate 3
This SubSeries is part of SuperSeries:
GSE71850 Blast traumatic brain injury induced cognitive deficits are attenuated by pre- or post-injury treatment with the glucagon-like peptide-1 receptor agonist, exendin-4
BioProject PRJNA292313

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE71846_RAW.tar 3.1 Mb (http)(custom) TAR
GSE71846_non-normalized.txt.gz 2.3 Mb (ftp)(http) TXT
Processed data included within Sample table
Raw data are available on Series record

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