Moderate noise induced cognition impairment of mice and its underlying mechanisms

Noise pollution is recognized as a serious human health problem in modern society. The aim of the present study was to explore the effects of moderate-intensity white noise exposure on learning and memory of mice, and the underlying mechanisms. The learning and memory ability of mice were evaluated by water maze and step-down inhibitory avoidance experiments respectively, following 1, 3, and 6 weeks noise exposure (80 dB SPL, 2 h/day). To explore potential mechanisms, we determined levels of oxidative stress in the inferior colliculus (IC), auditory cortex (AC), and hippocampus (the structures comprising the critical encephalic region associated with the acoustic lemniscal ascending pathway), the phosphorylation of microtubule-associated protein tau in the hippocampus (important role in learning and memory), and the basic auditory response properties of neurons in the IC. Moderate-intensity noise exposure impaired the learning and memory ability of mice in both water maze and step-down inhibitory avoidance experiments, and the longer the noise exposure time the greater the impairment. At 6 weeks after noise exposure, there was also evidence of oxidative damage in the IC, AC, and hippocampus, hyperphosphorylated tau protein in the hippocampus, and significant changes in the auditory response properties of neurons in the IC. These data results suggest that moderate-intensity noise can progressively impair the learning and memory ability of mice, which may result from peroxidative damage, tau hyperphosphorylation, and auditory coding alteration.

► Moderate-intensity noise was used in this study. ► Noise impaired the learning and memory ability of mice in a time-dependent manner. ► Noise induced oxidative damage in IC, AC and hippocampi. ► Noise induced hyperphosphorylation of tau protein in hippocampi. ► Noise caused the changes of auditory response properties in IC neurons.