EFFECTS OF ACUTE RESTRAINT-INDUCED STRESS ON GLUCOCORTICOID RECEPTORS AND BRAIN-DERIVED NEUROTROPHIC FACTOR AFTER MILD TRAUMATIC BRAIN INJURY
EFFECTS OF ACUTE RESTRAINT-INDUCED STRESS ON GLUCOCORTICOID RECEPTORS AND BRAIN-DERIVED NEUROTROPHIC FACTOR AFTER MILD TRAUMATIC BRAIN INJURY
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DOI：
10.1016/j.neuroscience.2012.03.005
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发表时间：
2012-05-17
期刊：
影响因子：
3.3
通讯作者：
Hovda, D. A.
中科院分区：
文献类型：
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作者：
Griesbach, G. S.;Vincelli, J.;Hovda, D. A.
我们以前曾报道，实验性轻度创伤性脑损伤导致在损伤后的第一周内对应激事件的敏感性增加，这是通过分析束缚诱导的应激后下丘脑-垂体-肾上腺(HPA)轴的调节来确定的。这是在轻度液压冲击伤(FPI)后康复运动被证明无效的同一时间段。在这里，我们评估了应激对神经可塑性的影响。成年雄性大鼠接受FPI或假损伤。另外一些大鼠只接受麻醉。大鼠暴露于束缚应激30min后，分别于伤后第1、7、14天采尾静脉血，并观察地塞米松(DEX)对其的影响。应激120min后取海马区组织。Western印迹法检测脑源性神经营养因子(BDNF)、糖皮质激素(GR)和盐皮质激素(MR)受体的表达。结果表明，糖皮质激素和盐皮质激素受体的损伤依赖性变化受地塞米松的影响。对照组和FPI大鼠对地塞米松的反应不同，因为在接受较低剂量的地塞米松治疗后，FPI组GR增加的持续时间更长。车辆处理组和假手术组的MR在PID1处受到抑制。在损伤后7、14天，不同的FPI组大鼠脑源性神经营养因子的前体形式减少。这些发现表明，轻度FPI后，损伤后第一周对应激事件的敏感性增加，对海马神经可塑性有影响。(C)2012年IBRO。爱思唯尔有限公司出版。保留所有权利。
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. (c) 2012 IBRO. Published by Elsevier Ltd. All rights reserved.