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作 者:Yang Ou Brad AClifton Jinghui Li David Sandlin Na Li Li Wu Chunming Zhang Tianwen Chen Jun Huang Yue Yu Jerome Allison Fan Fan Richard JRoman James Shaffery Wu Zhou Yi Pang Hong Zhu
机构地区:[1]Departmant of Otolaryngology and Head Neck Surgery [2]Department of Neurobiology and Anatomical Sciences [3]MD Program,School of Medicine [4]Graduate Program in Neuroscience [5]Department of Pediatrics [6]Department of Pharmacology and Toxicology [7]Department of Psychiatry and Human Behavior,University of Mississippi Medical Center,Jackson,MS,USA [8]Kunming Medical University,Kunming,Yunnan Province,China [9]Department of Otolaryngology,First Affiliated Hospital,Shanxi Medical University,Taiyuan,Shanxi Province,China
出 处:《Neural Regeneration Research》2022年第1期115-121,共7页中国神经再生研究(英文版)
基 金:supported by the National Institutes of Health(NIH)grants R21 DC017293(to HZ,WZ),R01 DC018919(to HZ,WZ),AG050049(to FF),AG057842(to FF),P20GM104357(to FF,RJR),and HL138685(to RJR)。
摘 要:Exposure to explosive shockwave often leads to blast-induced traumatic brain injury in military and civilian populations.Unprotected ears are most often damaged following exposure to blasts.Although there is an association between tympanic membrane perforation and TBI in blast exposure victims,little is known about how and to what extent blast energy is transmitted to the central nervous system via the external ear canal.The present study investigated whether exposure to blasts directed through the ear canal causes brain injury in LongEvans rats.Animals were exposed to a single blast(0–30 pounds per square inch(psi))through the ear canal,and brain injury was evaluated by histological and behavioral outcomes at multiple time-points.Blast exposure not only caused tympanic membrane perforation but also produced substantial neuropathological changes in the brain,including increased expression of c-Fos,induction of a profound chronic neuroinflammatory response,and apoptosis of neurons.The blast-induced injury was not limited only to the brainstem most proximal to the source of the blast,but also affected the forebrain including the hippocampus,amygdala and the habenula,which are all involved in cognitive functions.Indeed,the animals exhibited long-term neurological deficits,including signs of anxiety in open field tests 2 months following blast exposure,and impaired learning and memory in an 8-arm maze 12 months following blast exposure.These results suggest that the unprotected ear canal provides a locus for blast waves to cause TBI.This study was approved by the Institutional Animal Care and Use Committee at the University of Mississippi Medical Center(Animal protocol#0932 E,approval date:September 30,2016 and 0932 F,approval date:September 27,2019).
关 键 词:ANXIETY BLAST EAR ear protection learning memory MICROGLIA NEUROINFLAMMATION neuron rat traumatic brain injury
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