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Background & Objective: In this research, we study the simultaneous effects of Nitric Oxide (NO) and stress on prefrontal cortex of rats. Nitric Oxide is an unstable small molecule that involved in many physiological and pathological conditions. Brain’s prefrontal cortex has important role on personality and mental state. Its development continues after birth and this period is the most sensitive time for brain’s cortex to response to environmental parameters such as psychological stresses. Materials & Methods: In this study Wistar male rats received L-arginine (200 mg/kg) as NO precursor, L-NAME (20mg/kg) and 7-nitroindazole (25mg/kg) as non specific and specific NO sentries inhibitors. L-arginine and L-NAME were injected intra peritoneal (IP) and 7-nitroindazole injected subcutaneously (S.C) during one month per day. Rats divided in two groups (with stress and without stress). The kind of stress was immobilization every day for one month during injection of materials. Brains were removed after this period and each brain with a coronal section manner divided in two parts .Anterior part of brain fixed by formalin and tissue processing was done. By using rotatory microtome 10? serial cross sections were obtained and stained with H & E. Posterior part of brain homogenized with such solution then amount of NO in obtained solution was measured by spectrophotometer with 540 nm wavelength. Results: Statistical analysis of light microscopic findings indicated that stress of immobilization with use of L-NAME and 7-nitroindazole result in decrease of thickness of prefrontal cortex , numbers of Betz cells and NO production in rats’ brain, it means L-NAME and 7-nitroindazole exaggerate the brain damage and from other hands L-arginine with stress can convert these results. Conclusion: On the basis of these results we believe that stress of immobilization damages prefrontal cortex and also NOS inhibitors can aggravate the cortical damage. On the other hand although NO precursor (L-arginine) decreases the cortical damage in rats that impress with stress, it can result in these changes in rat’s brain without stress.

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Background & Objective: Many evidence indicated that action of glucocorticoid receptors can modulate anxiety behaviors and these effects probably mediated by nitric oxide (NO) system. Thus, in this study, we investigated interaction between corticosterone and NO on anxiety behaviors in mice in elevated plus maze (EPM).

Materials & Methods: In this experimental study male albino mice (25-30 g) were used. A standard EPM was used to determine anxiety behaviors. Two behavioral measures were used that include of the percentage of time spent in the open arms and the ratio of open arm entries to total entries during 5 min. Animals received IP injection of L-Name 30 mg/kg as an inhibitor or L-Arginine 50 mg/kg as a synthesis of NO or saline 60 min and corticosterone (1, 2.5, 5 mg/kg) 30 min before of evaluation.

Results: Analysis of data indicated that corticosterone at doses of 1 and 2.5, but not 5 mg/kg significantly reduced anxiety behavior in mice (P<0.05). Also pretreatment of L-Name potentiate but injection of L-Arginine had inhibition of corticosterone effects (P<0.05).

Conclusion: This study revealed that glucocorticoid induces anxiolytic effects and these effects probably potentiate by NO inhibitor and reduced by NO synthesis. Therefore, it seems that there are interaction between of glucocorticoid and NO system for control of anxiety behaviors.

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Background and Objective: Nitric oxide synthase (NOS) paly a role in nitric oxide (NO) generation. Despite the beneficial effects of NO on different body systems its overproduction of produce reactive nitrogen species (RNS) and nitrosilation of proteins. This study was done to evaluate the effect of asymmetric dimethylarginine (ADMA) and NG-Monomethyl-L-arginine methyl ester (L-NMMA) on inhibition of nitric oxide synthase activity. Materials and Methods: In this laboratory study, Nitric oxide synthase was extracted from 500 grams of sheep kidney by homogenization, ammonium sulphate precipitation and column chromatography on DEAE-32 Cellulose and 2', 5'-ADP-agarose. During purification, protein content was measured according to the Bradford and enzyme activity was assayed using the Griess reactions the inhibitory effects of 25 μΜ concentrations of ADMA and L-NMMA on purified enzyme were determined. Results: Specific activity and yield of NOS were 0.6 units/mg protein and 0.9%, respectively. Molecular weight of purified enzyme was 54 KD with SDS-PAGE. ADMA and L-NMMA in 25 μΜ concentrations reduced enzyme activity by 76 and 61.2%, respectively. Km values for NOS in absence and in presence of ADMA and L-NMMA were 5.32 μM, 31.25 μM (P<0.05) and 14.29 μM (P<0.05), respectively. Vmax for NOS in absence and presence of inhibitors was not changed. Conclusion: ADMA and L-NMMA have competitive inhibitory effect on NOS activity and ADMA have higher inhibitory effect than L-NMMA.