| Background:Sensorineural hearing loss (SNHL) is one of the most common neurological disorders affecting approximately 10% in adult human subjects and approximately 1.4 per 1000 of newborn babies. According to etiology, SNHL can be divided into two major categories:inherited-and acquired. Noise exposure is one of the major causes for acquired SNHL. In graduates from neonatal intensive care unit (NICU), 20%-40%show hearing loss. Roizen suggested that NICU noise is a highly risk factor for SNHL to those infants. Exposure to different types of noise during early childhood might have hazardous effects that are cumulative and shown off in adulthood. Noise exposure can impair physical and psychological health of children as well as their learning ability and cognitive performance. However, the underlying mechanisms are still unclear.Objective:To reveal the effect of noise induced hearing loss (NIHL) during early individual development in mice on the capabilities of learning and memory and the possible connection between the cognitive function and NIHL.Research methods:At postnatal day 15 (P15d), the animals-in the noise-group (n=47, group A) were exposed to a broadband (white)noise at 123 dB SPL for 2 h, while the animals in the control group (n=47, group B) accepted the sham exposure (environmental change) only. All observations were done two months after the noise exposure (at the age of 2.5 months).The hearing threshold was evaluated by using frequency specific auditory brainstem response (ABR). The capability of spatial learning and memory was measured by means of Morris water maze test. The neuronal proliferation in hippocampus was investigated by immunohistochemical labeling to the marker of immature neurons (doublecortin, DCX).The expression of two learning related immediate early genes (IEGs):Neuronal Per-Arnt-Sim domain protein 4(Npas4), activity-regulated cytoskeleton-associated protein(Arc)in hippocampus was measured by testing the mRNA using quantitative Reverse Transcription Polymerase Chain Reaction (qRT-PCR). The oxidative stress in hippocampus was-measured by testing the activity of superoxide dismutase (SOD), and the level of madondialdehyde (MDA) adduct.Results:As compared with the control group at 2 months after the noise exposure, a moderate degree of NIHL was induced in the group A by the single exposure to intense noise during early development:the frequency average of ABR threshold in the noise group was 70.07+2.122 dB SPL, significantly higher than the value of 42.02±0.6872 dB SPL obtained in the control group (Student t test, t40=15.26, P<0.0001), indicating a moderate hearing loss induced by the noise. The result of Morris water maze shows-that the spatial learning and memory in noise group-was poorer than that of the control. There is significant correlation between the hearing threshold and the capabilities of spatial learning and memory. The animals with NIHL shows reduced cell proliferation in hippocampus. The expression of Npas4 and Arc was significantly up regulated by spatial learning activity in both groups, lower in the noise group. However, the difference between the two groups did not reach statistical significance. No significant difference in oxidative stress represented by the level of SOD and MDA levels in hippocampus between the two groups, which were tested two month after the noise exposure.Conclusion:Independent of the oxidative stress, the hearing loss induced by a brief, intense noise exposure during early development in mice affected their capabilities in spatial learning and memory in adulthood, which is likely due to decrease of the decrease in learning related regulation of IEGs, followed by the depression of neurogenesis in hippocampus. |
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