Recovery of Chronic Noise Exposure Induced Spatial Learning and Memory Deficits in Young Male Sprague‐Dawley Rats

Abstract

Objective: Noise has always been an important environmental public health issue for mankind. Although reports exist on hippocampaldependent spatial learning and memory (LM) impairment due to noise, there are only a few studies that have examined the effects of recovery from noise stress on LM impairments. Therefore, the present study investigated the effects of recovery from chronic noise exposure on LM deficits. Materials and Methods: In this study, the detrimental effects of noise stress on young male rats in the Morris water maze (MWM) were investigated at 1, 10, 20, 30, and 40 days after the discontinuation of chronic noise exposure of 80 dB or 100 dB for 4 h per day, for 30 days. The levels of monoamine neurotransmitters in the hippocampus were also evaluated by HPLC-EC at the end of each behavioral test. Results: Statistical analysis revealed that rats in the noise-treated groups failed to reach the same level of performance as the controls in the MWM. Further, the levels of dopamine (DA), norepinephrine (NE) and 5-hydroxytryptamine (5-HT) were significantly decreased in the hippocampus after noise exposure. However, the reduction in monoamine levels and impaired water maze performance recovered over time, so that by 30th day after cessation of noise exposure the 80 dB group showed no performance difference from the controls, and by 40th day, the 100 dB group also showed no performance difference from the control. Conclusion:Our findings suggest that noise impaired LM in young male rats and reduced monoamine neurotransmitters in the hippocampus. However, the noise-induced water maze deficits recovered over time, and the concurrent restoration of hippocampal monoamine neurotransmitter levels suggest that they are involved in LM impairments. (J Occup Health 2011; 53: 157-163)

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

“…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).…”

Protective effect of the orientin on noise-induced cognitive impairments in mice

“…In the current study, orientin treatment markedly reversed the reductions of NE and DA induced by chronic noise exposure. The NE and DA neurotransmitter systems are involved in learning and memory processes, and a substantial part of learning and memory impairment is due to changes in neurotransmission [41]. Therefore, the reversal of the noise-induced alteration of the levels of NE and DA may contribute to orientin's effect in improving the cognitive impairments induced by chronic noise exposure.…”

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

“…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.…”

“…Noise exposure may induce the generation of free radicals and deplete the activities of antioxidant enzymes in plasma and tissues [10,11]. Previous studies have shown that increased oxidative stress is the cause of neuronal degeneration in auditory nuclei as well as the brain regions critical for cognitive functions [6,12,13].…”