Effects of Chronic Noise Exposure on Spatial Learning and Memory of Rats in Relation toThe purpose of this study was to examine the effects of noise exposure on spatial learning and memory and associated mechanisms in the hippocampus (HIP). Methods: Forty-eight male SD rats were grouped as: A, control; B, Morris water maze (MWM) training group; C, noise exposure group; and D, noise exposure followed by MWM training group. The influence of noise stress on spatial learning and memory in rats was assessed in hidden platform acquisition training and probe trial testing in MWM. Changes in morphology of Nissl bodies were observed in the CA1, CA3 and DG regions of HIP. In order to understand the possible mechanisms behind noise stress-induced changes, the concentration of amino acid neurotransmitters and the expression of NMDAR2B (NR2B) in HIP were also evaluated. Results: After noise exposure, the performance of spatial learning and memory in group D was decreased significantly compared to group B. The concentration of glutamate was significantly increased in groups C and D, whereas GABA decreased markedly. The mean optical density of Nissl bodies in groups C and D was reduced in the CA1, DG and CA3 regions. The expression of NR2B was significantly decreased in the CA1, CA3 and DG regions in group C, and in the CA1 and CA3 regions in group D as compared with groups A and B. Conclusions: Excitotoxicity, impaired Nissl bodies and reduced expression of NR2B in rat HIP induced by chronic noise exposure might have caused the impairment of spatial learning and memory. (J Occup Health 2009; 51: 152-158)

Chronic noise exposure has been implicated in increased risk of diabetes. However, there is limited experimental evidence of the mechanisms linking chronic noise stress and glucose metabolism. We addressed this in the present study by examining glucose metabolism, immune response, and changes in gut microbiota/host inflammatory homeostasis in rats exposed to noise for 30 consecutive days. Chronic noise exposure increased blood glucose and corticosterone levels for at least 14 days after cessation of noise. Stressed rats also exhibited elevated levels of glycogen and triglyceride in the liver and impaired hepatic insulin production via insulin-induced insulin receptor/insulin receptor substrate 1/glycogen synthase kinase 3β signalling, which persisted for 3–14 days after cessation of noise exposure. Chronic noise altered the percentage of Proteobacteria and Actinobacteria in the gut, increasing Roseburia but decreasing Faecalibacterium levels in the cecum relative to controls. Immunoglobulin A, interleukin 1β, and tumor necrosis factor α levels were also elevated in the intestine of these animals, corresponding to noise-induced abnormalities in glucose regulation and insulin sensitivity. These results suggest that lifelong environmental noise exposure could have cumulative effects on diabetes onset and development resulting from alterations in gut microbiota composition and intestinal inflammation.

BackgroundChronic noise exposure is associated with neuroinflammation and gut microbiota dysregulation and increases the risk of Alzheimer’s disease (AD). Environmental hazards are also thought to be associated with genetic susceptibility factors that increase AD pathogenesis. However, there is limited experimental evidence regarding the link between chronic noise stress and microbiome-gut-brain axis alterations, which may be closely related to AD development.MethodsThe aim of the present study was to systematically investigate the effects of chronic noise exposure on the microbiome-gut-brain axis in the senescence-accelerated mouse prone 8 (SAMP8) strain. We established SAMP8 mouse models to examine the consequences of noise exposure on the microbiome-gut-brain axis. Hippocampal amyloid-β (Aβ) assessment and the Morris water maze were used to evaluate AD-like changes, 16S ribosomal RNA sequencing analyses were used for intestinal flora measurements, and assessment of endothelial tight junctions and serum neurotransmitter and inflammatory mediator levels, as well as fecal microbiota transplant, was conducted to explore the underlying pathological mechanisms.ResultsChronic noise exposure led to cognitive impairment and Aβ accumulation in young SAMP8 mice, similar to that observed in aging SAMP8 mice. Noise exposure was also associated with decreased gut microbiota diversity and compositional alterations. Axis-series studies showed that endothelial tight junction proteins were decreased in both the intestine and brain, whereas serum neurotransmitter and inflammatory mediator levels were elevated in young SAMP8 mice exposed to chronic noise, similar to the observations made in the aging group. The importance of intestinal bacteria in noise exposure-induced epithelial integrity impairment and Aβ accumulation was further confirmed through microbiota transplantation experiments. Moreover, the effects of chronic noise were generally intensity-dependent.ConclusionChronic noise exposure altered the gut microbiota, accelerated age-related neurochemical and inflammatory dysregulation, and facilitated AD-like changes in the brain of SAMP8 mice.Electronic supplementary materialThe online version of this article (10.1186/s12974-018-1223-4) contains supplementary material, which is available to authorized users.

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