Background: Environmental noise is a known stressful factor, that induces alterations of various physiological responses in the exposed individuals. Extensive evidences from animal and human studies have indicated that stress influences cognitive functions. Studies have shown that chronic exposure to noise during pregnancy impairs neurobehavioral and reproductive functions and also reduces the body weight of the offspring. It seems that prenatal noise stress during last three months of fetal life damages the neurons in special areas of brain involved in cognition and impairs the activity of hypothalamuspituitary- adrenal (HPA) axis. It is known very little about the effect of prenatal noise stress on learning. The aim of present work was to determine the effect of prenatal chronic intermittent noise stress on learning in rats.Methods: Fifteen Wistar pregnant rats were exposed chronically to intermittent white noise (90-120 dB, 350 Hz) during the last two weeks of their pregnancy periods (dark cycle, 07:00Pm-07:00 Am). Stressed and no stressed puppies bred under normal condition up to 3 months of age. Both stressed and no stressed adult male and female rats were trained in an equal 3 arms Y-maze with 20-25 Volts D.C. electrical foot shock and a 12 Watts light stimuli as anactive voidance learning.Animals were trained one session daily and criterion condition response (CCR) was 90 percent of last session of training. Results: Data showed that chronic exposure to noise during pregnancy impairs learning of stressed male rats significantly at all sessions (P<0.01). However, in the stressed female rats the response was decreased significantly only at the first two sessions (P<0.05).Conclusion: The results indicate that prenatal noise stress may damage the neurons in special areas of brain such as hippocampus and alters cognition and behavioral functions.

Objectives: Noise is a potential environmental stressor affecting brain function as evidenced by altered stress neurotransmitters and hormone levels and psychobehavioral changes. Here, we explored the effects of noise exposure on the social behavior of mice as well as cerebral oxidative stress and neuroendocrine markers. Materials and Methods: In this experimental study, adult male mice were randomly allocated in; control-acute, acute-noise 90-dB, acute-noise 110-dB, control-chronic, chronic-noise 90-dB, and chronic-noise 110-dB groups. Animals in acute-and chronic-noise groups were exposed to 2 h/day of 90-or 110-dB white noise for one-day and three-month, respectively. At the end of the noise interventions, mice subjected to social interaction test. Also, serum levels of cortisol and cerebral malondialdehyde (MDA) levels, and superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities as well as total antioxidant capacity were measured. Results: Although mice in both acute noise 90-and 110-dB groups did not show any alteration in social behaviors and novel recognition performance, mice in chronic noise in 90-and 110-dB groups exhibited lower levels of mentioned behavioral paradigms. Moreover, these behavioral changes in the both chronic noise groups were accompanied by lower body weight, increased MDA levels, and decreased SOD and GPx activities, and reduced total antioxidant capacity levels. Interestingly, the acute noise increased brain MDA levels as well as enhanced SOD and GPx activities and total antioxidant capacity. Finally, we found lower serum cortisol levels in both acute and chronic groups. Conclusions: The noise exposure at levels ≥ 90-dB impairs sociability, associated with an imbalance of cerebral oxidative status and increased stress hormone.