1M.Sc. Student of Physiology, Physiology Research Center, Kashan University of Medical Sciences, Kashan, Iran
2Ph.D. Candidate, Physiology Research Center, Kashan University of Medical Sciences, Kashan, Iran
3Professor of Physiology, Physiology Research Center, Kashan University of Medical Sciences, Kashan, Iran
4Associate Professor of Physiology, Department of Physiology, School of Medicine, Kashan University of Medical Sciences, Kashan, Iran
Background: It is believed that cognitive processing is easily disturbed by incompatible environmental stimulations. Many studies have shown that prenatal stress affects fetal brain development. The aim of this study was to evaluate the effect of noise pollution exposure during conception period on neural activity of hippocampus CA1 area in male rat offspring. Methods: Four groups of rats including a control group with natural pregnancy and without any stress and three groups of pregnant rats exposed to daily noise stress (intensity >95 dB, between 8 A.M - 2 P.M) with durations of 1, 2 and 4 hour (s) in the last week of pregnancy were included in the study. Then, in male offsprings of these groups, fEPSP resulted from Schaffer collateral neurons of CA1 were recorded and evaluated in baseline state and after LTP induction with tetanic stimulation. Results: Our results showed that prenatal exposure to traffic noise pollution at 3rd gestational week, reduces amplitude (P<0.0001) and slope of baseline synaptic activity in hippocampus CA1 area (P<0.0001) and furthermore interferes in hippocampal LTP in comparison with control group. The serum level of corticostrone in the two stressed groups (2 and 4 hours) of rats in comparison to the control showed significant increase. But, prenatal exposure to 1- hour noise pollution caused no significant difference in serum corticostrone level. Conclusions: Based on the obtained results, daily exposure to noise pollution in the third trimester of pregnancy for 1, 2 and 4 hour (s), attenuates fEPSP features of hippocampus CA1 area pyramidal neurons of offsprings.