Impaired Learning Due to Noise Stress During Pregnancy in Rats Offspring

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 (90-120dB, 350Hz) during the last two weeks of their pregnancy periods (dark cycle, 07:00Pm-07:00Am). Stressed and nonstressed puppies bred under normal condition up to 3 months of age. Both stressed and nonstressed adult male and female rats were trained in an equal 3 arms Y-maze with 20-25 Volts D.C. electrical footshock and a 12 Watts light stimuli as an active avoidance 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. Keywords: noise stress, pregnancy, learning, rat

Effects of noise stress during fetal life on pain threshold in rats

Abstract: It has been shown that many types of physical-environmental stresses during fetal life alter behavioral responses to stimuli. Sex hormones have been shown to be evolved in these behavior. Nociception can also be affected by stress, but the mechanism(s) are not fully investigated. In this study NMRI pregnant rats (220-250 gr) were exposed to repetitive one hour intermittent noise stress (90-120 db, low frequency, white noise) during night dark cycle. Intensity and frequency of noise varied each 2-3 minutes between minimum and maximum levels. Pain threshold was measured after subcutaneous injection of 50µl formalin (2.5%) in right paw. The experiment considered to have tow stages: 1) phasic pain, minutes 0-15 and 2) tonic pain minutes 20-50. Pain score was marked every 15 seconds. The results showed that exposing to noise stress during fetal life has mostly affected tonic pain threshold. Pain threshold in stressed female offspring was increased significantly compared to stressed male offspring or compared to control male and female offspring. In conclusion it is suggested that noise stress during fetal life may increase pain threshold (Hypoalgesia). Increase in endogenouse opioid release may be considered as the mechanism. Keywords: Noise stress, Pain threshold, Fetal life, Formalin test, Offspring rat

Effect of Short-term Forced Exercise on Naloxone Induced Withdrawal Symptoms in Morphine Addicted Male Rats

ABSTRACT: Introduction & Objective: Opioid dependence has been causing limitation in usage of morphine and other opioid drugs in pain control. The aim of this study was to assess the effect of short-term forced exercise on withdrawal syndrome in morphine addicted male rats. Materials & Methods: This experimental study was done in the physiology research center of Ahwas Jondishapour University of Medical Sciences. Twenty four young male Wistar rats, weighing 200-300gr, were randomly divided into four groups: no addiction and no exercise, no addiction and exercise, addiction and no exercise and addiction and exercise. The exercise groups underwent treadmill forced exercise for ten days. The first five days morphine was administrated (ip) twice daily with increasing dose (5، 10، 20، 40, 50 mg/kg) to addicted groups. Also single dose (50mg/kg) of morphine was administrated to them on the 10th day of exercise. After administration of naloxone hydrochloride the withdrawal symptoms were evaluated for 5 minutes. The findings of this study were analyzed by SPSS software and One- way ANOVA (Tukey) test. Results: The findings of this study showed that the withdrawal symptoms was elevated in exercise and addicted groups in comparison with control group (p<0.05 , p<0.01). However, most of withdrawal symptoms decreased in addicted and exercise group in comparison with addicted and no exercise group (p<0.01, p<0.001). Conclusion: The exercise could increase endogenous opioid and withdrawal symptoms in animals but reduce withdrawal symptoms in addicted and exercise groups compared to addicted and no exercise group. Its mechanism might be related to down regulation and low sensitivity of opioid receptor

Riboflavin may ameliorate neurological motor disability but not spatial learning and memory impairments in murine model of multiple sclerosis

Summary: Background & aims: Riboflavin has an important role in myelin formation. This experimental study assesses the interactions between the effects of riboflavin and interferon beta-1a (INF-β1a) on motor disability, spatial learning and memory, and brain-derived neurotrophic factor (BDNF) in experimental autoimmune encephalomyelitis (EAE). Methods: In the present research C57BL/6 mice (n = 56) were divided into sham and treatment groups. Riboflavin was administrated (10 mg/kg/day) orally for two weeks alone and/or combined with INF-β1a at 150 IU/g of body weight. After the induction of EAE, the animals were investigated for the clinical signs. Spatial learning and memory were assessed through the standard Morris water maze (MWM). The brain and spinal cord levels of BDNF were studied using real-time polymerase chain reactions and enzyme-linked immunosorbent assay. The data were analyzed using one-way ANOVA, repeated measures, and generalized estimating equations model. Results: The results in the brain revealed that BDNF mRNA expression (P < 0.01) and protein levels (P < 0.05) increased in the EAE mice treated with the combination of riboflavin and INF-β1a compared to the treated groups with riboflavin or INF-β1a. Clinical scores were reduced in groups treated with riboflavin compared to other groups. EAE mice treated with riboflavin swam significantly faster in MWM compared to other groups (P < 0.05). No significant differences were found between EAE and healthy mice in other spatial learning and memory evaluating variables. Conclusion: The data highlighted the synergistic role of riboflavin and INF-β1a in improving the disability but not spatial learning and memory mediated by BDNF in EAE. Keywords: Riboflavin, Experimental autoimmune encephalomyelitis, Brain-derived neurotrophic factor, Memor