Abstract
Exposure of developing rats to noise has shown to induce hippocampal-related behavioral alterations that were prevented after a week of housing in an enriched environment. However, neither the effect of repeated exposures nor its impact on key endogenous antioxidants had been studied yet. Thus, the aim of the present work was to reveal novel data about hippocampal oxidative state through the measurement of possible age-related differences in the levels of hippocampal thioredoxins in rats exposed to noise at different developmental ages and subjected to different schemes and housing conditions. In addition, the possibility that oxidative changes could underlie hippocampal-related behavioral changes was also analyzed. Developing male Wistar rats were exposed to noise for 2 h, either once or for 5 days. Upon weaning, some animals were transferred to an enriched cage for 1 week, whereas others were kept in standard cages. One week later, auditory and behavioral assessments, as well as measurement of hippocampal thioredoxin, were performed. Whereas no changes in the auditory function were observed, significant behavioral differences were found, that varied according to the age, scheme of exposure and housing condition. In addition, a significant increase in Trx-1 levels was found in all noise-exposed groups housed in standard cages. Housing animals in an enriched environment for 1 week was effective in preventing most of these changes. These findings suggest that animals become less susceptible to undergo behavioral alterations after repeated exposure to an environmental challenge, probably due to the ability of adaptation to an unfavorable condition. Moreover, it could be hypothesized that damage to younger individuals could be more easily prevented by a housing manipulation.
Highlights
We have reported that EE was able to prevent noise-induced behavioral alterations in PND28 animals exposed at PND7 and PND15 to noise for 2 h (Molina et al, 2016a), data in animals exposed for 5 days have not been obtained yet
No significant changes in auditory brainstem responses (ABRs) thresholds in any of the frequencies tested were observed in PND28 animals exposed to noise at PND7 and PND15 [non-parametric Kruskall–Wallis test, H < 4 and p > 0.05 (NS) for all frequencies, Figures 2A,B]
Data show that exposure to noise at PND7, according to N1 and N5 schemes, induced a decrease in the number of lines crossed in the second session of the Open Field Task (OF) when compared with the first session, both in standard or in enriched conditions, that resulted similar to what was observed in sham animals, when evaluated at PND28 [Figure 3A, N1: Three-way analysis of variance (ANOVA), F(7,65) = 7.77, p < 0.01
Summary
Data from the literature have shown that exposure to noise could be capable to induce damage to the auditory system (Frenzilli et al, 2004; Gourévitch et al, 2014) as well as to structures of different extra-auditory tissues, such as brain structures (prefrontal cortex and hippocampus), cardiac tissues or adrenal and thyroid glands (Trapanotto et al, 2004; Manikandan et al, 2006; Uran et al, 2010; Gannouni et al, 2013; Molina et al, 2016a; Miceli et al, 2018). It has been reported that exposure to noise was able to induce changes in the cochlear oxidative state (Yamane et al, 1995; Yamasoba et al, 1998; Dehne et al, 2000; Yamashita et al, 2004; Fetoni et al, 2015). Ohlemiller et al (1999) reported a significant increase in ROS cochlear levels 1 h after exposure to noise, even when the acoustic stimulus is no longer present and Tamura et al (2012) found that oxidative stress might be induced in the Corti organ of the inner ear after noise exposure in a rodent animal model. Kurioka et al (2014) reported an increase in mitochondrial ROS production and excitotoxicity in the cochlea of rats exposed to noise
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