PMID- 22445725 OWN - NLM STAT- MEDLINE DCOM- 20120921 LR - 20211021 IS - 1873-7544 (Electronic) IS - 0306-4522 (Print) IS - 0306-4522 (Linking) VI - 210 DP - 2012 May 17 TI - Effects of acute restraint-induced stress on glucocorticoid receptors and brain-derived neurotrophic factor after mild traumatic brain injury. PG - 393-402 LID - 10.1016/j.neuroscience.2012.03.005 [doi] AB - We have previously reported that experimental mild traumatic brain injury results in increased sensitivity to stressful events during the first post-injury weeks, as determined by analyzing the hypothalamic-pituitary-adrenal (HPA) axis regulation following restraint-induced stress. This is the same time period when rehabilitative exercise has proven to be ineffective after a mild fluid-percussion injury (FPI). Here we evaluated effects of stress on neuroplasticity. Adult male rats underwent either an FPI or sham injury. Additional rats were only exposed to anesthesia. Rats were exposed to 30 min of restraint stress, followed by tail vein blood collection at post-injury days (PID) 1, 7, and 14. The response to dexamethasone (DEX) was also evaluated. Hippocampal tissue was collected 120 min after stress onset. Brain-derived neurotrophic factor (BDNF) along with glucocorticoid (GR) and mineralocorticoid (MR) receptors was determined by Western blot analysis. Results indicated injury-dependent changes in glucocorticoid and mineralocorticoid receptors that were influenced by the presence of dexamethasone. Control and FPI rats responded differentially to DEX in that GR increases after receiving the lower dose of DEX were longer lasting in the FPI group. A suppression of MR was found at PID 1 in vehicle-treated FPI and Sham groups. Decreases in the precursor form of BDNF were observed in different FPI groups at PIDs 7 and 14. These findings suggest that the increased sensitivity to stressful events during the first post-injury weeks, after a mild FPI, has an impact on hippocampal neuroplasticity. CI - Copyright (c) 2012 IBRO. Published by Elsevier Ltd. All rights reserved. FAU - Griesbach, G S AU - Griesbach GS AD - Department of Neurosurgery, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA. ggriesbach@mednet.ucla.edu FAU - Vincelli, J AU - Vincelli J FAU - Tio, D L AU - Tio DL FAU - Hovda, D A AU - Hovda DA LA - eng GR - R01 NS061960/NS/NINDS NIH HHS/United States GR - NS6190/NS/NINDS NIH HHS/United States GR - R01 NS061960-04/NS/NINDS NIH HHS/United States GR - R01 NS061960-02/NS/NINDS NIH HHS/United States GR - R01 NS061960-01A2/NS/NINDS NIH HHS/United States GR - R01 NS061960-02S1/NS/NINDS NIH HHS/United States GR - R01 NS061960-03/NS/NINDS NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't DEP - 20120315 PL - United States TA - Neuroscience JT - Neuroscience JID - 7605074 RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (Glucocorticoids) RN - 0 (Receptors, Glucocorticoid) RN - 0 (Receptors, Mineralocorticoid) RN - 7S5I7G3JQL (Dexamethasone) SB - IM MH - Animals MH - Blotting, Western MH - Brain Injuries/*complications/*metabolism MH - Brain-Derived Neurotrophic Factor/*metabolism MH - Dexamethasone/pharmacology MH - Glucocorticoids/pharmacology MH - Hippocampus/drug effects/metabolism MH - Male MH - Neuronal Plasticity MH - Rats MH - Rats, Sprague-Dawley MH - Receptors, Glucocorticoid/*metabolism MH - Receptors, Mineralocorticoid/metabolism MH - Restraint, Physical MH - Stress, Psychological/*complications/*metabolism PMC - PMC3358418 MID - NIHMS369121 EDAT- 2012/03/27 06:00 MHDA- 2012/09/22 06:00 PMCR- 2013/05/17 CRDT- 2012/03/27 06:00 PHST- 2011/10/31 00:00 [received] PHST- 2012/02/23 00:00 [revised] PHST- 2012/03/04 00:00 [accepted] PHST- 2012/03/27 06:00 [entrez] PHST- 2012/03/27 06:00 [pubmed] PHST- 2012/09/22 06:00 [medline] PHST- 2013/05/17 00:00 [pmc-release] AID - S0306-4522(12)00217-5 [pii] AID - 10.1016/j.neuroscience.2012.03.005 [doi] PST - ppublish SO - Neuroscience. 2012 May 17;210:393-402. doi: 10.1016/j.neuroscience.2012.03.005. Epub 2012 Mar 15.