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.

Background: The hippocampus is responsible for memory. A diet full of antioxidants improves brain damage and cognitive function.Regard the antioxidant effects of zingiber officinalis (ginger) and its flavonoids components.Objectives: The aim of this study was to evaluate the effect of the extract of ginger on memory by using hippocampus tissue of the male offspring of rats.Materials and Methods: In this study, 60 rats, 15 males and 45 females, were used. We separated pregnant female rats from males on the first day of pregnancy (determined by vaginal plug), and during days 16 - 18 of pregnancy, via intraperitoneal injection, three groups received hydroalcoholic extract of ginger, with low (200 mg/kg bw), medium (400 mg/kg bw), and high (800 mg/kg bw) concentration doses. The control group did not receive anything, and the sham group received normal saline during these days.Then at day 50, the males offspring in each group were sacrificed, their brains were removed, and the hippocampus sections were prepared for microscopic studies. Data was analyzed by SPSS 20 and by using one-way ANOVA and then a Tukey post-test (P<0.05 considered as the significance level).Results: This research showed that the number and thickness of pyramidal and granular layers of the CA1 and dentate gyrus areas of the hippocampus had increased in male offspring according to the increase in the ginger extract dose.Conclusions: It seems as though ginger extract, which contains compounds such as gingerols, shogaols, and zingerone, can affect memory ability in rats through these compounds’ antioxidant properties by affecting embryonic acetylcholine content and place cells.

Background: The consequences of exposure to mercury and its compounds on the reproductive potential and health of offspring are a pressing problem for the global scientific community. The purpose of this study was to examine the effect of mercury chloride toxicity in the parent rats on the postnatal development, behavior, and neuromuscular conductivity of their adult offspring. Methods: The experiments were conducted in parental Wistar rats of both sexes, which were subcutaneously injected daily with mercury chloride solution (HgCl2) at a rate of 0.5 mg/kg before mating for 6 weeks. We assessed the postnatal mortality, body weight, surface righting reflex and motor activity of the newborn offspring. The examination of the adult offspring included open field, resident-intruder and rotarod tests, development of the food-procuring reflex, and electro-neuromyography examinations. Results: The study results showed that exposure to HgCl2 in parental rats of both sexes before mating resulted in low motor activities and failure of impulse conduction in the neuromuscular apparatus of the hind limbs in the offspring. In addition, maternal exposure to HgCl2 before mating led to failure of the cognitive abilities in the adult offspring while the paternal exposure led to a decline in the offspring’s aggressiveness. Conclusion: The study results supported the need for further investigation on the long-term effects of mercury toxicity on the rats’ generations, and the mechanism of transmission of the "chemical load" from generation to generation.

Background and Objectives: Hippocampus is the main structure involved in spatial learning and memory consolidation. Formation of spatial memory can be strongly influenced by medications, hormones and different substances. Due to importance of new pharmacotherapy on drug administration in pregnancy, the aim of this study was to investigate the effect of letrozole-therapy during pregnancy on memory and learning in offspring rats. Methods: In this study, 24 pregnant rats were divided into a control and three experimental groups (N=6). The subjects received low dose (0. 25 mg/Kg), average dose (0. 5 mg/Kg) and high dose (1 mg/Kg) of letrozole orally during 16-19 days of gestation. After maturating, learning and memory of the offspring were assessed by passive avoidance learning apparatus. Data were analyzed by SPSS 20 using one-way analysis of variance and the Tukey's test. P-values less than 0. 05 were considered statistically significant. Results: Weights of the offspring who received letrozole decreased significantly compared with the control. There was no significant difference in the step-through latency between the experimental groups. However, the step-through latency and time spent in the dark compartment decreased significantly in the experimental groups compared with control group (P<0. 05). Conclusion: The results of this study show that letrozole can influence learning and memory of offspring rats.

Purpose: It seems that maternal intervention, which may involve epigenetic mechanisms, can affect cerebral ischemia in offspring. Metformin consumption by the mother activates the AMP-activated protein kinase (AMPK) pathway. Metformin has also induced the AMPK and protected neurons in cerebral ischemia. This study investigates the effect of maternal metformin administration, which activates the AMPK pathway, on cerebral ischemia in offspring. Methods: Animals were separated into four groups: sham, 2-vessels occlusion (2VO), Met+2VO, Met+compound c (CC)+2VO. Female rats were administrated with metformin at a dose of 200 mg. kg-1 body weight for 2 weeks prior to mating. After the final metformin injection, each female rat was paired with an intact adult male to allow for mating. Sixty-days old offspring underwent cerebral ischemia and then memory-related tests were done. Results: Current data revealed that the neurological deficits score was reduced Met+2VO group (P<0. 001), and the memory increased (P<0. 001) in comparison to the 2VO. The Bcl-2/Bax ratio declined in the metformin group (P<0. 001) while the brain-derived neurotropic factor (BDNF), c-fos, p-AMPK/AMPK ratio and Histone H3K9 acetylation in the hippocampus augmented significantly compared to the 2VO group (P<0. 001). Conclusion: These findings indicated that the metformin intervention via AMPK activation could improve the movement disability, enhance spatial memory, increase neural plasticity, and augment the bioenergetics state and histone acetylation in the hippocampus of the offspring.