TRPV4-induced Neurofilament Injury Contributes to Memory Impairment after High Intensity and Low Frequency Noise Exposures.

Yang Yang; Ju Wang; Yu Lian Quan; Chuan Yan Yang; Xue Zhu Chen; Xue Jiao Lei; Liang Tan; Hua Feng; Fei LI; Tu Nan Chen

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TRPV4-induced Neurofilament Injury Contributes to Memory Impairment after High Intensity and Low Frequency Noise Exposures.

Author: Yang YANG ^{1
,

2} ; Ju WANG ³ ; Yu Lian QUAN ³ ; Chuan Yan YANG ³ ; Xue Zhu CHEN ³ ; Xue Jiao LEI ³ ; Liang TAN ³ ; Hua FENG ³ ; Fei LI ³ ; Tu Nan CHEN ³
Author Information

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 904th Hospital of PLA, School of Medicine of Anhui Medical University, Wuxi 214044, Jiangsu, China.
3. Department of Neurosurgery and Key Laboratory of Neurotrauma, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing 400038, China.
Publication Type:Journal Article
Keywords: Hippocampus; Low frequency noise; Memory impairment; Nerve fibers; Neurofilament; TRPV4
MeSH: Animals; Mice; TRPV Cation Channels/metabolism*; Intermediate Filaments/metabolism*; Hippocampus/metabolism*; Neurons/metabolism*; Memory Disorders/metabolism*
From: Biomedical and Environmental Sciences 2023;36(1):50-59
CountryChina
Language:English
Abstract: 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 HI-LFN.
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 neurofilament-positive nerve fibers in the cornu ammonis 1 (CA1) and dentate gyrus (DG) hippocampal areas in wild-type 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.