Impulse noise exposure in rats causes cognitive deficits and changes in hippocampal neurotransmitter signaling and tau phosphorylation

Cui, Bo; Wu, Mingquan; She, Xiaojun; Liu, Hongtao

doi:10.1016/j.brainres.2011.08.035

Cited by 66 publications

(52 citation statements)

References 39 publications

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“…The current data provide no additional evidence that natural hearing loss (presbycusis), which is highly correlated with age, contributes independently to redox changes. This stands in potential contrast with previous studies demonstrating that direct induction of acoustic trauma using noise stimuli also produce general cognitive changes in experimental animals (Cernak, et al, 2001, Cui, et al, 2012). It is important to note in this context that the relationship, if any, between the redox changes seen in CA2 and CA3 in the current study, and cognitive performance, is not yet known.…”

Section: 0 Discussioncontrasting

confidence: 99%

The impact of aging, hearing loss, and body weight on mouse hippocampal redox state, measured in brain slices using fluorescence imaging

Stebbings

Choi

Ravindra

et al. 2016

Neurobiology of Aging

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The relationships between oxidative stress in the hippocampus and other aging-related changes such as hearing loss, cortical thinning or changes in body weight are not yet known. We measured the redox ratio in a number of neural structures in brain slices taken from young and aged mice. Hearing thresholds, body weight and cortical thickness were also measured. We found striking aging-related increases in the redox ratio that were isolated to the stratum pyramidale, while such changes were not observed in thalamus or cortex. These changes were driven primarily by changes in FAD, not NADH. Multiple regression analysis suggested that neither hearing threshold nor cortical thickness independently contributed to this change in hippocampal redox ratio. However, body weight did independently contribute to predicted changes in hippocampal redox ratio. These data suggest that aging-related changes in hippocampal redox ratio are not a general reflection of overall brain oxidative state, but are highly localized, while still being related to at least one marker of late aging, weight loss at the end of life.

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Section: 0 Discussioncontrasting

confidence: 99%

The impact of aging, hearing loss, and body weight on mouse hippocampal redox state, measured in brain slices using fluorescence imaging

Stebbings

Choi

Ravindra

et al. 2016

Neurobiology of Aging

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“…As Mc2r is the sole receptor for ACTH, this observation may provide insight into how environmental noise exposure may modulate the stress response of the hippocampus. Studies elsewhere have reported that chronic environmental noise exposure is associated with disrupted function of the hippocampus, an extra-auditory structure of the central nervous system, thereby inducing memory deficit and cognition impairment (Cheng et al, 2011;Chengzhi et al, 2011;Manikandan et al, 2006;Uran et al, 2012Uran et al, , 2010Cui et al, 2012Cui et al, , 2013. Indeed, Jáuregui-Huerta et al showed that chronic exposure to environmental noise in the early stages of life produces a long-lasting reduction in cell proliferation in the hippocampus in the neurogenic and non-neurogenic hippocampal regions (Kraus and Canlon, 2012).…”

Section: Discussionmentioning

confidence: 97%

Effects of environmental noise exposure on DNA methylation in the brain and metabolic health

Guo

et al. 2017

Environmental Research

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Environmental noise exposure is associated with adverse effects on human health including hearing loss, heart disease, and changes in stress-related hormone levels. Alteration in DNA methylation in response to environmental exposures is a well-known phenomenon and it is implicated in many human diseases. Understanding how environmental noise exposures affect DNA methylation patterns may help to elucidate the link between noise and adverse effects on health. In this pilot study we examined the effects of environmental noise exposure on DNA methylation of genes related to brain function and investigated whether these changes are related with metabolic health. We exposed four groups of male Wistar rats to moderate intensity noise (70-75dB with 20-4000Hz) at night for three days as short-term exposure, and for three weeks as long-term exposure. Noise exposure was limited to 45dB during the daytime. Control groups were exposed to only 45dB, day and night. We measured DNA methylation in the Bdnf, Comt, Crhr1, Mc2r, and Snca genes in tissue from four brain regions of the rats (hippocampus, frontal lobe, medulla oblongata, and inferior colliculus). Further, we measured blood pressure and body weight after long-term noise exposure. We found that environmental noise exposure is associated with gene-specific DNA methylation changes in specific regions of the brain. Changes in DNA methylation are significantly associated with changes in body weight (between Bdnf DNA methylation and Δ body weight: r=0.59, p=0.018; and between LINE-1 ORF DNA methylation and Δ body weight: =-0.80, p=0.0004). We also observed that noise exposure decreased blood pressure (p=0.038 for SBP, p=0.017 for DBP and p 0. 017 for MAP) and decreased body weight (β=-26g, p=0.008). In conclusion, environmental noise exposures can induce changes in DNA methylation in the brain, which may be associated with adverse effects upon metabolic health through modulation of response to stress-related hormones.

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“…Noise exposure exceeds 90 dB has been reported to be a source of stressor [4]. The adverse impact of noise on learning, memory and hippocampal neurogenesis has been reported by previous studies [5][6][7][8][9]. The mechanisms underlying the decline of memory after noise exposure are not entirely clear.…”

Section: Introductionmentioning

confidence: 95%

Neuroprotective effects of Tualang honey against oxidative stress and memory decline in young and aged rats exposed to noise stress

Azman

Zakaria

Othman

et al. 2018

Journal of Taibah University for Science

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The neuroprotective effects of Tualang honey in stress-induced young and aged rats were investigated. Tualang honey (200 mg/kg body weight) was administered for 28 days. Stressinduced rats were subjected to loud noise 100 dB(A) 4 hours daily for 14 days. Stress exposure significantly induced memory impairment, increased brain oxidation indices, and decreased antioxidant enzymes activities and neuronal density in mPFC, CA2 and CA3 hippocampal areas in both young and aged rats. The stressed rats treated with Tualang honey showed a significant decrease in stress hormone levels and brain oxidation indices, and increase in memory, antioxidant enzymes activities, and neuronal density in mPFC and hippocampus compared to the vehicle-treated stressed rats. The protective effect of Tualang honey was more prominent in young than aged rats. These results suggest the neuroprotective effects of Tualang honey against oxidative stress and memory decline due to stress exposure and/or ageing through its antioxidant property. ARTICLE HISTORY

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Impulse noise exposure in rats causes cognitive deficits and changes in hippocampal neurotransmitter signaling and tau phosphorylation

Cited by 66 publications

References 39 publications

The impact of aging, hearing loss, and body weight on mouse hippocampal redox state, measured in brain slices using fluorescence imaging

The impact of aging, hearing loss, and body weight on mouse hippocampal redox state, measured in brain slices using fluorescence imaging

Effects of environmental noise exposure on DNA methylation in the brain and metabolic health

Neuroprotective effects of Tualang honey against oxidative stress and memory decline in young and aged rats exposed to noise stress

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