RGD Reference Report - Decreased neuroinflammation and increased brain energy homeostasis following environmental enrichment after mild traumatic brain injury is associated with improvement in cognitive function. - Rat Genome Database

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Decreased neuroinflammation and increased brain energy homeostasis following environmental enrichment after mild traumatic brain injury is associated with improvement in cognitive function.

Authors: Briones, TL  Woods, J  Rogozinska, M 
Citation: Briones TL, etal., Acta Neuropathol Commun. 2013 Sep 6;1:57. doi: 10.1186/2051-5960-1-57.
RGD ID: 11565089
Pubmed: PMID:24252176   (View Abstract at PubMed)
PMCID: PMC3893439   (View Article at PubMed Central)
DOI: DOI:10.1186/2051-5960-1-57   (Journal Full-text)

BACKGROUND: Persistent neuroinflammation and disruptions in brain energy metabolism is commonly seen in traumatic brain injury (TBI). Because of the lack of success of most TBI interventions and the documented benefits of environmental enrichment (EE) in enhancing brain plasticity, here we focused our study on use of EE in regulating injury-induced neuroinflammation and disruptions in energy metabolism in the prefrontal cortex and hippocampus. Adult male Wistar rats were used in the study and randomly assigned to receive either: mild TBI (mTBI) using the controlled cortical injury model or sham surgery. Following surgery, rats from each group were further randomized to either: EE housing or standard laboratory housing (CON). After 4 weeks of recovery, cognitive testing was performed using the non-matching-to-sample and delayed non-matching-to-sample tasks. After completion of behavioral testing, levels of the pro-inflammatory cytokines IL-1beta and TNF-alpha and the anti-inflammatory cytokine IL-10 were measured. In addition, levels of AMPK (adenosine monophosphate-activated protein kinase), phosphorylated AMPK and uMtCK (ubiquitous mitochondrial creatine kinase) were assessed as measures of brain energy homeostasis. RESULTS: Our results showed that EE: (1) decreased the pro-inflammatory cytokines IL-1beta and TNF-alpha and enhanced levels of the anti-inflammatory cytokine IL-10 after mTBI; (2) mitigated mTBI-induced cognitive impairment; and (3) attenuated mTBI-induced downregulation in pAMPK/AMPK ratio and uMtCK levels. CONCLUSIONS: Our data demonstrated the potential of EE to modulate the persistent: (1) neuroinflammatory response seen following mTBI, and (2) persistent disturbance in brain energy homeostasis. It is possible that through the mechanism of modulating neuroinflammation, EE housing was able to restore the disruption in energy metabolism and enhanced functional recovery after mTBI.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Brain Injuries treatmentISOCkmt1 (Rattus norvegicus)11565089; 11565089 RGD 
Brain Injuries treatmentIEP 11565089 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Ckmt1  (creatine kinase, mitochondrial 1)

Genes (Mus musculus)
Ckmt1  (creatine kinase, mitochondrial 1, ubiquitous)

Genes (Homo sapiens)
CKMT1B  (creatine kinase, mitochondrial 1B)


Additional Information