| Popis: |
Background: Excessive exposure to high-intensity, low-frequency noise (HI-LFN) causes vibroacoustic disease (VAD). Memory deficits is one non-auditory symptomatic effect found in humans and rodents with VAD, but the mechanism is largely unknown. This study was designed to explore the nerve fibers impairment in hippocampus and potential mechanism after HI-LFN exposure.Methods: HI-LFN injury model was established by exposing to noises with a frequency of 100, 150 or 200 Hz and a pressure level of 140dB. Adult male WT and TRPV4-/- mice were employed in present study. After HI-LFN exposure, the new object recognition task and the morris water maze were used for examining the memory impairment, HE staining was used to examine the holistic morphological changes hippocampus, immunofluorescence and western blot were used to the detect the change of nerve fibers in dentate gyrus (DG) and CA1 of the hippocampus.Results: The expression of TRPV4 was significantly upregulated in hippocampus after HI-LFN exposure. What’s more, prominent learning and memory deficits and lower neural cell density with injured nerve fibers in CA1 and DG areas of hippocampus were found in WT mice after HI-LFN exposure. However, TRPV4-/- mice showed better performance in learning and memory tests and more integrated nerve fibers in CA1 and DG areas after HI-LFN exposure compared with that in WT mice.Conclusions: Our data indicated a novel mechanism that the injury of neurons and nerve fibers in hippocampus might be the primary trigger of memory deficits after HI-LFN exposure, and TRPV4 activation plays crucial role in the injury of neurons and nerve fibers in hippocampus, those findings provide a promising therapeutic target for treating cognitive dysfunction after low frequency noise exposure. |
