@article{ref1,
title="Unexpected role of stress as a possible resilience mechanism upon mild traumatic  brain injury (mTBI) in mice",
journal="Molecular and cellular neurosciences",
year="2020",
author="Shavit-Stein, Efrat and Gerasimov, Alexandra and Aharoni, Shay and Gofrit, Shany G. and Pikus, Ellen and Pick, Chaim G. and Maggio, Nicola",
volume="ePub",
number="ePub",
pages="ePub-ePub",
abstract="INTRODUCTION: Mild traumatic brain injury (mTBI) is common and associated with  cognitive impairment. Stress and mTBI are known to modulate the neural function. The  present study aims at exploring the effect of prior stress exposure on cognitive  function following mTBI. <br><br>METHODS: Eight weeks old male ICR mice were subjected to  either stress induced by forced swimming stress alone, stress followed by an  immediate mTBI, or stress followed by 30 minutes break and then mTBI. We had two  control groups: SHAM group - a control group which was not exposed to stress nor to  mTBI and control mTBI group - a control group which was exposed only to TBI with no  stress. Mice were weighted prior and at 12, 24 hours and 1 week following  interventions. Motor evaluation was conducted by rotarod. Behavioral changes were  evaluated using open field, Y maze, elevated plus maze and staircase tests, at 12  hours and 1 week following interventions. Brain levels of NMDAR subunits (R1, R2A,  R2B), GABA(B)R1, glucocorticoid and mineralocorticoid receptors (GR, MR) were  evaluated using western blot. <br><br>RESULTS: Stress alone, mTBI alone, and stress followed  by immediate mTBI resulted in a significant weight loss compared to control  (p<0.05). Stress 30 minutes prior to mTBI had a protective effect on weight (p=0.14  compared to control). The stress and mTBI alone groups showed reduced time at the  center of the open field arena 1 week after intervention (p<0.05 for both). Time in  the novel arm of the Y maze was significantly shorter in the mTBI and stress  followed by delayed mTBI (p=0.02). Immediate stress prior to mTBI had normalized  times in the novel arm (p=0.95 compared to control). Combination of stress and mTBI  significantly modified NMDAR subunits levels (increased NMDAR1, p<0.008, decreased  NMDAR2A p=0.02) as well as increased MR levels (p=0.04). <br><br>CONCLUSION: Exposure to  stress prior to mTBI may improve the cognitive consequences of mTBI. These data may  point towards a novel, unexpected role of stress as a possible resilience mechanism  in the setting of mTBI.<p /> <p>Language: en</p>",
language="en",
issn="1044-7431",
doi="10.1016/j.mcn.2020.103586",
url="http://dx.doi.org/10.1016/j.mcn.2020.103586"
}