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作 者:YANG Yang WANG Ju QUAN Yu Lian YANG Chuan Yan CHEN Xue Zhu LEI Xue Jiao TAN Liang FENG Hua LI Fei CHEN Tu Nan
机构地区:[1]Department of Neurosurgery and Key Laboratory of Neurotrauma,Southwest Hospital,Third Military Medical University(Army Medical University),Chongqing 400038,China [2]Department of Neurosurgery,The 904h Hospital of PLA,School of Medicine of Anhui Medical University,Wuxi 214044,Jiangsu,China
出 处:《Biomedical and Environmental Sciences》2023年第1期50-59,共10页生物医学与环境科学(英文版)
基 金:funded by the Chongqing Postdoctoral Innovative Talent Support Program[Grant No.CQBX2021008];the Chongqing Talents Project[CQYC202105043]。
摘 要:Objective Exposure to high intensity, low frequency noise(HI-LFN) causes vibroacoustic disease(VAD),with memory deficit as a primary non-auditory symptomatic effect of VAD. However, the underlying mechanism of the memory deficit is unknown. This study aimed to characterize potential mechanisms involving morphological changes of neurons and nerve fibers in the hippocampus, after exposure to HILFN.Methods Adult wild-type and transient receptor potential vanilloid subtype 4 knockout(TRPV4^(-/-)) mice were used for construction of the HI-LFN injury model. The new object recognition task and the Morris water maze test were used to measure the memory of these animals. Hemoxylin and eosin and immunofluorescence staining were used to examine morphological changes of the hippocampus after exposure to HI-LFN.Results The expression of TRPV4 was significantly upregulated in the hippocampus after HI-LFN exposure. Furthermore, memory deficits correlated with lower densities of neurons and neurofilamentpositive nerve fibers in the cornu ammonis 1(CA1) and dentate gyrus(DG) hippocampal areas in wildtype mice. However, TRPV4^(-/-)mice showed better performance in memory tests and more integrated neurofilament-positive nerve fibers in the CA1 and DG areas after HI-LFN exposure.Conclusion TRPV4 up-regulation induced neurofilament positive nerve fiber injury in the hippocampus,which was a possible mechanism for memory impairment and cognitive decline resulting from HI-LFN exposure. Together, these results identified a promising therapeutic target for treating cognitive dysfunction in VAD patients.
关 键 词:Low frequency noise Memory impairment TRPV4 NEUROFILAMENT Nerve fibers HippocampusLow frequency noise Memory impairment TRPV4 NEUROFILAMENT Nerve fibers HIPPOCAMPUS
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