Cognitive improvement of mice induced by exercise prior to traumatic brain injury is associated with cytochrome c oxidase

Gu, Ying; Zhang, Li wei; Ma, Ning; Ye, Lin lin; Wang, De xin; Gao, Xu

doi:10.1016/j.neulet.2014.04.004

Cited by 27 publications

(16 citation statements)

References 24 publications

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“…EX-TBI mice exhibited a significant decrease in spatial learning memory deficits when compared to NOEX-TBI mice at 7 days post-TBI. This finding is in agreement with Gu et al, who showed that 3 weeks of pre-TBI voluntary wheel running attenuated spatial learning memory deficits in mice at 15 days post-TBI, and diminished neuron and synaptic density loss resulting from the injury (Gu et al, 2014). Griesbach et al, revealed that a delayed initiation (i.e., 14 days post-TBI) of post-TBI exercise enhanced spatial learning memory after injury (Griesbach et al, 2009).…”

Section: Discussionsupporting

confidence: 92%

Exercise preconditioning improves traumatic brain injury outcomes

et al. 2015

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Purpose-To determine whether 6 weeks of exercise performed prior to traumatic brain injury (TBI) could improve post-TBI behavioral outcomes in mice, and if exercise increases neuroprotective molecules (vascular endothelial growth factor-A [VEGF-A], erythropoietin [EPO], and heme oxygenase-1 [HO-1]) in brain regions responsible for movement (sensorimotor cortex) and memory (hippocampus). Methods-120 mice were randomly assigned to one of four groups: 1) no exercise + no TBI (NOEX-NOTBI [n=30]), 2) no exercise + TBI (NOEX-TBI [n=30]), 3) exercise + no TBI (EX-NOTBI [n=30]), and 4) exercise + TBI (EX-TBI [n=30]). The gridwalk task and radial arm water maze were used to evaluate sensorimotor and cognitive function, respectively. Quantitative real time polymerase chain reaction and immunostaining were performed to investigate VEGF-A, EPO, and HO-1 mRNA and protein expression in the right cerebral cortex and ipsilateral hippocampus.Results-EX-TBI mice displayed reduced post-TBI sensorimotor and cognitive deficits when compared to NOEX-TBI mice. EX-NOTBI and EX-TBI mice showed elevated VEGF-A and EPO mRNA in the cortex and hippocampus, and increased VEGF-A and EPO staining of sensorimotor cortex neurons 1 day post-TBI and/or post-exercise. EX-TBI mice also exhibited increased VEGF-A staining of hippocampal neurons 1 day post-TBI/post-exercise. NOEX-TBI mice demonstrated increased HO-1 mRNA in the cortex (3 days post-TBI) and hippocampus (3 and 7 days post-TBI), but HO-1 was not increased in mice that exercised.Conclusions-Improved TBI outcomes following exercise preconditioning are associated with increased expression of specific neuroprotective genes and proteins (VEGF-A and EPO, but not HO-1) in the brain.

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Section: Discussionsupporting

confidence: 92%

Exercise preconditioning improves traumatic brain injury outcomes

et al. 2015

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“…Numerous studies involving small animal models of TBI have described changes in synaptic protein levels following TBI; commonly utilized models include fluid percussion or controlled cortical injury 47–50 . These studies describe both reductions and increases in SYP protein after TBI in hippocampus and cortical regions measured over a range of times after injury, from 1 day to 30 days.…”

Section: Discussionmentioning

confidence: 99%

Exendin-4 attenuates blast traumatic brain injury induced cognitive impairments, losses of synaptophysin and in vitro TBI-induced hippocampal cellular degeneration

Rachmany

Tweedie

Rubovitch

et al. 2017

Sci Rep

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Mild blast traumatic brain injury (B-TBI) induced lasting cognitive impairments in novel object recognition and less severe deficits in Y-maze behaviors. B-TBI significantly reduced the levels of synaptophysin (SYP) protein staining in cortical (CTX) and hippocampal (HIPP) tissues. Treatment with exendin-4 (Ex-4) delivered by subcutaneous micro-osmotic pumps 48 hours prior to or 2 hours immediately after B-TBI prevented the induction of both cognitive deficits and B-TBI induced changes in SYP staining. The effects of a series of biaxial stretch injuries (BSI) on a neuronal derived cell line, HT22 cells, were assessed in an in vitro model of TBI. Biaxial stretch damage induced shrunken neurites and cell death. Treatment of HT22 cultures with Ex-4 (25 to 100 nM), prior to injury, attenuated the cytotoxic effects of BSI and preserved neurite length similar to sham treated cells. These data imply that treatment with Ex-4 may represent a viable option for the management of secondary events triggered by blast-induced, mild traumatic brain injury that is commonly observed in militarized zones.

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“…After development, they were rinsed in distilled water, dehydrated in an ascending series of ethanol, cleared in Neoclear (Harleco, Gibbstown, NJ, USA), and coverslipped in the dark to dry for 1.5 weeks. Neurons for analysis were chosen on the basis as described previously (Hoffman et al 2011;Gu et al 2014). Diameter of somata, dendritic length, and basal/apical branch points were also quantified.…”

Section: Golgi Stainingmentioning

confidence: 99%

“…Somata diameter and spine density were analyzed using a two-way ANOVA, followed by Mann-Whitney U test. P values less than 0.05 were considered being significant (Gu et al 2014).…”

Section: Golgi Stainingmentioning

confidence: 99%

miR21 is Associated with the Cognitive Improvement Following Voluntary Running Wheel Exercise in TBI Mice

Zhou²,

Chang

et al. 2015

J Mol Neurosci

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Recent evidences revealed that the alteration of microRNAs (miRNAs) might be associated with neuroplasticity induced by voluntary running wheel (RW) exercise in mice suffered from traumatic brain injury (TBI). In the present study, we explored the possible role of miR21 involved in the cognitive improvement following voluntary RW in TBI mice. Firstly, in situ hybridization and quantitative real-time PCR (qRT-PCR) were employed to determine the hippocampal expression and location of miR21 in TBI mice with or without spontaneous RW. Either miR21-mimics/plenti-miR21 or miR21-agomir/miR21-sponge was employed to regulate the miR21 expression in vivo and in vitro. Acquisition of spatial learning and memory retention was assessed by Morris Water Maze (MWM) test. Golgi stain was also performed to evaluate the alteration of hippocampal dendrite. Our finding confirmed that the elevated miR21 level in hippocampal post-TBI was significantly reduced by spontaneous RW. Overexpression of miR21 in TBI mice with spontaneous RW induced deteriorations in spatial learning and memory retention by significant decreases in the somata size and branch points of the hippocampus neurons. In vitro transduction with miR21 also reduced the neurite extension and the area of cultured hippocampal neuron. However, miR21 down-regulation reversed these effects. The present data strongly suggest that miR21 is an important molecule that has been involved in neuroprotection induced by voluntary RW exercise post-TBI.

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Cognitive improvement of mice induced by exercise prior to traumatic brain injury is associated with cytochrome c oxidase

Cited by 27 publications

References 24 publications

Exercise preconditioning improves traumatic brain injury outcomes

Exercise preconditioning improves traumatic brain injury outcomes

Exendin-4 attenuates blast traumatic brain injury induced cognitive impairments, losses of synaptophysin and in vitro TBI-induced hippocampal cellular degeneration

miR21 is Associated with the Cognitive Improvement Following Voluntary Running Wheel Exercise in TBI Mice

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