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Inadequate Expression and Activation of Mineralocorticoid Receptor Aggravates Spatial Memory Impairment after Traumatic Brain Injury.

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收录情况： ◇ SCIE

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机构： [a]Beijing Key Laboratory of Central Nervous System Injury, Beijing Neurosurgical Institute, Capital Medical University, Beijing, China [b]Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China [c]Nerve Injury and Repair Center of Beijing Institute for Brain Disorders, Beijing, China [d]China National Clinical Research Center for Neurological Diseases, Beijing, China [e]Department of Neurosurgery, Tianjin Fifth Center Hospital, Tianjin, China [f]Department of Ultrasound, Beijing Tian Tan Hospital, Capital Medical University, Beijing, China

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摘要：

The administration of glucocorticoids (GCs) for the treatment of traumatic brain injury (TBI) is controversial. Both protective and deleterious effects of GCs on the brain have been reported in previous studies, while the mechanisms are unclear. Most experimental studies have reported glucocorticoid receptor (GR)-mediated deleterious effects after TBI. Sufficient mineralocorticoid receptor (MR) activation was reported to be indispensable for normal function and survival of hippocampal neurons, but changes in MR expression and activation and the roles of MRs in the survival of neurons after TBI remain unclear. We hypothesized that inadequate MR expression and activation caused by TBI aggravates posttraumatic hippocampal apoptosis but that restoration by restoring MRs promotes the survival of neurons. Using a rat controlled cortical impact model, we examined plasma corticosterone, MR expression and activation, neuronal apoptosis in the hippocampus, and spatial memory on day 3 after injury with and without fludrocortisone (1 mg/kg) treatment. Plasma corticosterone levels were significantly reduced after TBI. In addition, both MR expression and activation were inhibited. Fludrocortisone treatment significantly increased both the expression and activation of MRs, reduced the number of apoptotic neurons and cell loss in the ipsilateral hippocampus, and subsequently improved spatial memory. Its protective effects were counteracted by the MR antagonist spironolactone. The results suggest that adequate expression and activation of MRs is crucial for the survival of neurons after TBI and that fludrocortisone protects hippocampal neurons via promoting MR expression and activation. Copyright © 2019 IBRO. Published by Elsevier Ltd. All rights reserved.

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出版当年[2018]版：

大类 | 3 区医学

小类 | 3 区神经科学

最新[2023]版：

大类 | 3 区医学

小类 | 4 区神经科学

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出版当年[2017]版：

Q2 NEUROSCIENCES

最新[2023]版：

Q2 NEUROSCIENCES

影响因子： 2.9 最新[2023版] 3 最新五年平均 3.382 出版当年[2017版] 3.362 出版当年五年平均 3.277 出版前一年[2016版] 3.244 出版后一年[2018版]

第一作者：

第一作者机构： [b]Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China

通讯作者：

通讯机构： [a]Beijing Key Laboratory of Central Nervous System Injury, Beijing Neurosurgical Institute, Capital Medical University, Beijing, China [b]Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China [c]Nerve Injury and Repair Center of Beijing Institute for Brain Disorders, Beijing, China [d]China National Clinical Research Center for Neurological Diseases, Beijing, China [*1]Department of Neurosurgery, Beijing Tian tan Hospital, Capital Medical University, No. 119 Nan Si Huan W. Road, Fengtai District, Beijing 100070, China.

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