Tehran University Medical Journal

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Background: Learning and memory are the complicated agents of central nervous system that various regions of brain can be involved in these phenomena, especially regions like hippocamp. Various agents like nitric oxide and morphine can influence learning and memory. About the effects of morphine with other components there was not clear reports so in this study the effect of co-administration of L-Arginine (precursor of nitric oxide) and morphine in hippocampal CA3 area on spatial learning and memory in male rats was investigated.
Methods: Male rats were deeply anaesthetized with ketamine and xylazine and cannula were implanted bilaterally in CA3 of hippocampus by using streotaxic technique, Then male rats were used in seven groups that received saline, L-Arginine (0/3M), L-Arginine (3μg/rat), L-NAME (0/3M), morphine (10mg/rat), L-Arginine (3μg/rat) with morphine or L-NAME with morphine for five days that they were trained in morris water maze to evaluate spatial learning and memory. There was a control group too.
Results: Our results showed that L-Arginine (3μg/rat) improved spatial learning and memory. L-NAME (inhibitor of nitric oxide) decreased spatial learning and memory in male rats. Injection of morphine also decreased spatial learning and memory in male rats. Co-administeration of L-NAME and morphine decreased learning more than morphine individually in male rats.
Conclusion: We concluded that precursor of nitric oxide improved learning and memory in male rats and inhibitor of it and morphine impaired this phenomena and coadministration of inhibitor of nitric oxide and morphine also impaired learning in rats.

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Normal 0 false false false EN-US X-NONE AR-SA MicrosoftInternetExplorer4 Background: Neuronal injury in hippocampus is the most common pathological finding in temporal lobe epilepsy, accounting for approximately 70% of cases in patients with epilepsy. Neuroprotective effects of aspirin have been described in several neurodegenerative diseases. The aim of this study was to explore effects of aspirin on morphology and number of pyramidal neurons in CA1 and Dentate Gyrus area of hippocampus of rats in kindling model of epilepsy.
Methods: We divided the rats into t hree groups (n=8). Two groups received aspirin (30 mg/kg, p.o.) and saline, one week before and during induction of kindling. Kindling was induced in these groups by administration of pentylenetetrazole (PTZ: 40 mg/kg, ip). The third group received only saline throughout the study and served as health control group. After induction of kindling animals were sacrificed by perfusion with 10% saline solution under anesthesia. Histopathologic study of hippocampus were performed by light microscopy using H&E staining.
Results: A large number of injured pyramidal neurons with pyknotic nuclei and high eosinophilic cytoplasm are seen in CA1 and DG area of hippocampus of epileptic control group. Aspirin group had pyramidal neurons with clear nuclei and less density cytoplasm, similar to health control group (p<0.05). In kindled animals the number of intact pyramidal neurons in these two regions were significantly reduced and this effect was counteracted by aspirin (p<0.05).
Conclusions: Results of present study suggest that aspirin have neuroprotective effect against neuronal damage of hippocampus of kindled animals.

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Background: Depression, as one of the most prevalent and disabling disorders in the world, has a complex and yet not well-known pathophysiology. Genetic, hormonal, neurotransmitter, inflammatory and neurodegenerative theories are all responsible. Studies show that depression leads to structural changes in the hippocampus, prefrontal cortex, amygdala, anterior cingulate, and basal bodies. Hippocampal volume loss is observed due to the death of nerve cells, neurons, and glial cells, and reduced neurogenesis. The hippocampus is a part of the limbic system. The limbic system is the area in the brain that is associated with memory, emotions, and motivation. The limbic system is located just above the brain stem and below the cortex. Despite the many studies related to the reduced hippocampal neurogenesis in depressed patients, no study has compared the amount of neurodegeneration between the left and right hippocampus. In this study, we compared neurodegeneration levels in the right and left hippocampus of the rats. Methods: Twenty male Sprague-Dawley rats that were purchased Razi Institute, Karaj, Iran, were evaluated in the study. This study was conducted in cellular and molecular center in Iran University of Medical Sciences, from June 2012 to June 2013. Half of them had unpredictable chronic mild stress (UCMS) for 21 days to develop depression. The forced-swimming test (FST) was used to measure the immobility time (IB), a symptom of depression. One week after the behavioral test, the rats were prepared for transcardial perfusion. Then, paraffin fixed brain was excised and the hippocampus was prepared for Nissl staining. All above-mentioned procedures were performed for the control group too except inducing UCMS. Results: Our results increased IB in the UCMS group, 68.8 second in stress group and 15.1 second in control group. Nissl staining showed prominent neural degeneration in the hippocampus of the rats in the UCMS group. Comparison of the left and right hippocampal cells revealed that the right hippocampus (mean= 49.166) was more vulnerable to stress than the left hippocampus (mean= 76.6). Conclusion: Our study showed different manifestations of depression after UCMS. It showed that UCMS could lead to mental depression. This study showed that the right hippocampus was more sensitive to stress than the left hippocampus. In fact, UCMS resulted in depression. The study showed that the right hippocampus was more sensitive to stress than the left hippocampus. Therefore, the main function of the right hemisphere, which is adaptation to the new environment, is disturbed more.

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Background: Environmental signals have an essential role in the maturation of neural circuits during critical period of brain development. It has been shown that, change in visual signals during critical period of brain development changes structure and function of glutamate receptors in the visual cortex. After processing in visual cortex, part of visual signals goes to the hippocampus and makes memories. The aim of this study was evaluating effects of visual deprivation during critical period of brain development on AMPA receptor subunits expression in rats’ hippocampus. Methods: This experimental study was done in Physiology Research Center, Kashan University of Medical Sciences at winter 2014 on male Wistar rats. Animals were divided to 2 groups (n= 36 for each) were kept in standard 12 hours light/12 hours dark condition (light reared, LR) or in complete darkness (dark reared, DR) from birth to the end of the experiments. Using reverse transcription polymerase chain reaction (RT-PCR) and Western blotting techniques respectively, expression of mRNA and protein of GluR1 and GluR2 subunits was evaluated in rats’ hippocampus at ages 2, 4 and 6 weeks in both groups. After quantification of the expressions, the data were compared by two way analysis of variance. Results: The relative expression of GluR1 subunit decreased about 24% (P=0.004) in the hippocampus of 6 WLR rats in comparison to 2 WLR ones. The relative expression of the other AMPA receptor subunit, GluR2, also increased about 190% in the hippocampus of the 6WLR animals when compared to the 2 WLR rats (P< 0.0001). Dark rearing increased the relative expression of both subunits of AMPA receptors, GluR1 and GluR2, about 20 percent (P= 0.01) in the hippocampus of 6 WDR rats in comparison to 2 WLR animals. Conclusion: Dark rearing of rats during critical period of brain development changes the relative expression and also arrangement of both AMPA receptor subunits, GluR1 and GluR2 in the hippocampus, age dependently.

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Background: Seladin-1 protein protects the neural cells against amyloid beta toxicity and its expression decreased in vulnerable regions of Alzheimer's disease (AD) brains. On the other hand, changes in serum levels of S100 have been considered as a marker of brain damage in neurodegenerative diseases. Furthermore, this study was carried out to determine the relation between the change profile of serum S100&beta protein levels and hippocampal Seladin-1 gene expression in a rat model of sporadic AD. Methods: In this experimental study that established in Department of Neuroscience, School of Advanced Technologies in Medicine, Tehran University of Medical Science, from March 2011 to April 2013, 72 animals were randomly divided into control, 4, 7, 14, and 21days ICV-STZ/Saline administrated rats. Alzheimer's model was induced by intracerebroventricular (ICV) injections of streptozotocin (STZ) [3 mg/kg] on days 1 and 3. Serum levels of S100&beta and hippocampal Seladin-1 gene expression were evalu-ated in experimental groups. The initial and step-through latencies (STL) were deter-mined using passive avoidance test. Results: Serum levels of S100&beta were significantly different between the STZ-7 day and STZ-14 day groups in comparison with the control, saline and STZ-4 day groups. As well as, there was a significant difference between the STZ-7 day group in comparison with the STZ-14 day and STZ-21 day groups (P=0.0001). Hippocampal Seladin-1 gene expression in STZ-14 day and STZ-21 day groups significantly decreased as compared to the control, saline and STZ-4 day groups (P=0.0001). However, significant correla-tion was detected between serum S100&beta protein decrement and Seladin-1 down regula-tion (P=0.001). Also, the STL was significantly decreased in 21 days ICV-STZ adminis-trated rats as compared to the control or saline groups (P=0.001). Conclusion: Monitoring the changes of serum S100&beta protein levels by relationship with changes in hippocampal Seladin-1 gene expression can be a useful indicator of neu-ronal damage in patients with Alzheimer's disease.

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