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




Decreased neuroinflammation and increased brain energy homeostasis following environmental enrichment after mild traumatic brain injury is associated with improvement in cognitive function - Download this document for free, or read online. Document in PDF available to download.

Acta Neuropathologica Communications

, 1:57

First Online: 06 September 2013Received: 05 July 2013Accepted: 16 August 2013

Abstract

BackgroundPersistent 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-1β and TNF-α 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.

ResultsOur results showed that EE: 1 decreased the pro-inflammatory cytokines IL-1β and TNF-α 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.

ConclusionsOur 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.

KeywordsIL-β TNF-α IL10 AMPK Non-matching-to-sample task Electronic supplementary materialThe online version of this article doi:10.1186-2051-5960-1-57 contains supplementary material, which is available to authorized users.

Download fulltext PDF



Author: Teresita L Briones - Julie Woods - Magdalena Rogozinska

Source: https://link.springer.com/



DOWNLOAD PDF




Related documents