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Pathophysiological and behavioral deficits in developing mice following rotational acceleration-deceleration traumatic brain injury

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单位: [1]Department of Spine Surgery,Orthopedics Hospital affiliated to the Second Bethune Hospital, Jilin University, Changchun 130041, China. [2]Department of Pediatrics, University of Louisville School of Medicine, Louisville, KY 40202, USA. [3]Norton Neuroscience Institute, Norton Healthcare, Louisville, KY 40202, USA. [4]Department of Orthopedics, China-Japan Union Hospital of Jilin University, Changchun 130033, China. [5]Department of Neurological Surgery, China-Japan Friendship Hospital, Beijing 100029, China. [6]Eye Center of the Second Bethune Hospital, Jilin University, Changchun 130041, China. [7]Stark Neurosciences Research Institute, Department of Neurological Surgery, Indiana University School of Medicine, Indianapolis, IN 46202, USA. [8]Department of Neurological Surgery, University of Louisville School of Medicine, Louisville, KY 40202, USA. [9]Department of Anatomical Sciences and Neurobiology, University of Louisville School of Medicine, Louisville, KY 40202, USA.
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关键词: Abusive head trauma Shaken baby syndrome Rotational acceleration-deceleration injury Ischemia Hemorrhage Neuronal degeneration

摘要:
Abusive head trauma (AHT) is the leading cause of death from trauma in infants and young children. An AHT animal model was developed on 12-day-old mice subjected to 90 degrees head extension-flexion sagittal shaking repeated 30, 60, 80 and 100 times. The mortality and time until return of consciousness were dependent on the number of repeats and severity of the injury. Following 60 episodes of repeated head shakings, the pups demonstrated apnea and/or bradycardia immediately after injury. Acute oxygen desaturation was observed by pulse oximetry during respiratory and cardiac suppression. The cerebral blood perfusion was assessed by laser speckle contrast analysis (LASCA) using a PeriCam PSI system. There was a severe reduction in cerebral blood perfusion immediately after the trauma that did not significantly improve within 24 h. The injured mice began to experience reversible sensorimotor function at 9 days postinjury (dpi), which had completely recovered at 28 dpi. However, cognitive deficits and anxiety-like behavior remained. Subdural/subarachnoid hemorrhage, damage to the brain-blood barrier and parenchymal edema were found in all pups subjected to 60 insults. Proinflammatory response and reactive gliosis were upregulated at 3 dpi. Degenerated neurons were found in the cerebral cortex and olfactory tubercles at 30 dpi. This mouse model of repetitive brain injury by rotational head acceleration-deceleration partially mimics the major pathophysiological and behavioral events that occur in children with AHT. The resultant hypoxia/ischemia suggests a potential mechanism underlying the secondary rotational acceleration-deceleration-induced brain injury in developing mice.

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出版当年[2017]版:
大类 | 2 区 医学
小类 | 2 区 病理学 3 区 细胞生物学
最新[2025]版:
大类 | 3 区 医学
小类 | 2 区 病理学 3 区 细胞生物学
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出版当年[2016]版:
Q1 PATHOLOGY Q2 CELL BIOLOGY
最新[2023]版:
Q1 PATHOLOGY Q2 CELL BIOLOGY

影响因子: 最新[2023版] 最新五年平均[2021-2025] 出版当年[2016版] 出版当年五年平均[2012-2016] 出版前一年[2015版] 出版后一年[2017版]

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第一作者单位: [1]Department of Spine Surgery,Orthopedics Hospital affiliated to the Second Bethune Hospital, Jilin University, Changchun 130041, China. [2]Department of Pediatrics, University of Louisville School of Medicine, Louisville, KY 40202, USA.
通讯作者:
通讯机构: [1]Department of Spine Surgery,Orthopedics Hospital affiliated to the Second Bethune Hospital, Jilin University, Changchun 130041, China. [2]Department of Pediatrics, University of Louisville School of Medicine, Louisville, KY 40202, USA. [3]Norton Neuroscience Institute, Norton Healthcare, Louisville, KY 40202, USA. [8]Department of Neurological Surgery, University of Louisville School of Medicine, Louisville, KY 40202, USA. [9]Department of Anatomical Sciences and Neurobiology, University of Louisville School of Medicine, Louisville, KY 40202, USA.
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