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Introduction: There are evidences showing the role of nitric oxide in the opiate reward properties. The role of nitric oxide signaling pathway as an intracellular mechanism on augmentation of long term potentiation in hippocampal CA1 area of rats is also confirmed. It has been also reported that oral morphine dependence facilitates formation of spatial learning and memory via activation of NMDA receptors located in hippocampal CA1 area of rats. The effect of nitric oxide within hippocampal CA1 area on the spatial learning and memory processes in morphine dependent rats is unclear. Methods: 33 N-MRI male rats (250-350 g) were divided into 4 experimental groups. Two cannulae were stereotaxically implanted bilaterally into hippocampal CA1 area. After 5 days recovery, animals received morphine sulfate or sucrose for 30 consecutive days in drinking water. Morris water maze (MWM) studies were performed from day 26 to 30. In this period animals received bilateral intra-hippocampal CA1 injection of 3μg/ 2 μl L-NAME (NOS inhibitor) or 2 μl saline (1 μl/site), 1 min before daily experimentation. Spatial learning and memory parameters were subjected to analysis of variance (ANOVA). Results: Morphine dependence facilitated spatial learning and memory in rats. This effect was inhibited with local administration of L-NAME in hippocampal CA1 area. Conclusion: Activation of intracellular NO signaling pathway in the pyramidal cells of hippocampal CA1 area may involve in facilitating spatial learning and memory in morphine dependent rats.

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Introduction: Neurohormones like testosterone and estradiol have an important role in learning and memory. The hippocampus is essentially involved in learning and memory, and is known to be a target for estradiol actions. Estrogen receptors (ERs) are highly expressed in CA1 of rat hippocampus, and mediate the effects of estrogen on learning and memory. Estradiol receptor belong to a family of transcription factors, the nuclear receptor superfamily, and has two subtypes ER
and ER. The current research has been conducted to assess the effect of ER selective agonist, diarylpropionitrile (DPN), on passive avoidance of adult male rats, by using passive avoidance task.

Methods: Male adult rats were bilaterally cannulated into the CA1 area of hippocampus, and then received vehicle (dimethyl sulfoxide, DMSO) or DPN (0.2, 0.5, 1 micro-g/0.5 micro-l/side), 30 min before training on passive avoidance task.

Results: The results showed that pre-training intra-CA1 injections of DPN (0.5, 1 micro-g/0.5 micro-l/side), significantly decreased step-through latencies and increased time spent in dark on passive avoidance learning (P<0.01).

Conclusion: Our data suggest that intra-CA1 administration of DPN could impair learning and memory acquisition on passive avoidance task. 

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Introduction: Sub-chronic swim stress is known to induce a prolonged hyperalgesia, which is mediated through NMDA and opioid systems. Nitric oxide is a soluble gas, which acts as a retrograde messenger that modulates the release of mentioned neurotransmitters. It is also involved in nociception and memory. The aim of this study was to evaluate the role of NO pathway in nociception and memory disruption induced by sub-chronic swim stress. Methods: Three sessions forced swimming stress protocols were applied to rats. Before each swimming session, pretreatment with L-NAME (10 mg/kg, i.p.), L-Arginine (10 mg/kg, i.p.) or saline was made. Passive avoidance learning, nociception and anxiety-like behavior were evaluated 24 hours after last swim stress session. Results: Results showed that step through latency was decreased after swim stress and it could be inhibited by pretreatment with L-NAME. Swim stress increased anxiety-like behavior in the open field test, which could be inhibited by pretreatment with L-NAME and L-Arginine. Reduced thermal threshold was observed in the nociceptive measurement after swim stress. Pretreatment with L-NAME could reverse this reduced threshold. Conclusion: The results of this study indicate that sub-chronic swim stress impairs nociception and passive avoidance learning. It seems that NO pathway have a modulatory role in these alterations.

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Introduction: Many studies have shown that asthma is characterized by inflammation of the airway and infiltration of eosinophil cells (EOSCs). It has also shown that during pregnancy, the level of leptin, as a regulator of immune responses, increases with the progression of the pregnancy process. In this study, the effect of asthma on inflammatory factors was evaluated in the lung and uterine tissues of asthmatic pregnant or non-pregnant mice.
Methods: In this experimental study, 40 female Balb/c mice (8 weeks old) were classified into 4 groups, and asthma by ovalbumin (OVA) at a concentration of 20 μg/100μl was induced. Lung and uterus tissues were histopathologically evaluated for the presence of inflammation. The level of leptin hormone in blood serum was investigated using an indirect enzyme-linked immunosorbent assay (ELISA). Also, Interleukin-8 (IL-8), forkhead box protein 3 (Foxp3), eosinophil chemotactic protein (eotaxin), and mucin 5AC (Muc5ac) gene expression were measured in respiratory and uterine cells by Real-Time Quantitative Reverse Transcription PCR (qRT-PCR) assay (P<0.05, P<0.01 and P<0.001). 
Results: Morphological assessment of inflammation in lung tissue showed a significant increase in asthmatic groups compared to healthy groups. Hormone measurement revealed a significant rise in leptin levels in pregnant groups compared to non-pregnant groups. Also, the expression level of IL-8, Foxp3, eotaxin, and Muc5ac genes increased in pregnancy compared to negative control.
Conclusion: In asthma, inflammation rate increases at the cellular and molecular levels, and the leptin increment might have an influence on the inflammation.

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Introduction: The objective of the study was to find out the influence of Thioflavin-T (ThT) on obesity and fatty liver by investigating the adipokine hormones, and insulin serum level of male NMRI mice which were exposed to a high-fat diet (HFD).
Methods: 50 adult male NMRI mice were separated into five groups: n=10. The control group was given a standard diet at twelve-week intervals. The sham group was nourished with HFD that lasted for 8 weeks, afterwards, the group received a standard diet and solvent water (0.5ml) by gavage (4 weeks). The experimental groups 1-3 were nourished with HFD (4% cholesterol, 60% fat) eight-week period. Then, the treatment period started in experimental groups by receiving a normal diet in addition to ThT with three doses (5,10 and 15 mg/kg, 0.5ml), via gavage (4 weeks). 
Results: HFD contributed to a substantial reduction in serum adiponectin levels and increased leptin serum in the sham group opposite to the control group (P< 0.001). However, the concentration of both adipokine hormones was significantly modified under the treatment of ThT in a dose-dependent manner. Insulin serum increased in the sham group significantly (P< 0.001), meanwhile, a significant decrease was shown in experimental groups 2, and 3 than in the sham group (P<0.01). ThT also reduced HOMA-IR in experimental groups. The introduction of ThT in varying doses led to the induction of polymorphonuclear cells in the liver tissue.
Conclusion: Our findings propose that ThT can affect liver function and body weight by modulating the serum levels of adipokine hormones besides decreasing the level of insulin and HOMA-IR in mice fed with HFD.