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Background & Objective: Bombesin (BBS) is a tetra-decapeptide amino acid neuropeptide in central nervous system within a variety of mammalian species. Also it has many biological effects that may be effective in modulation of anxiety. The aim of present study was to determine the effect of BBS on modulation anxiety reaction in elevated plus maze (EPM) in mice.

 

Materials & Methods: 60 male mice (25-30 g) were used in this study. Bombesin in doses of 1.25, 2.5, 5, 10 and 20 µg/kg IP or saline was injected in different groups 10 min before of evaluation. Five minutes later for increase of activity, animal was put in black box for 5 min. Then each animal in regulated time transferred to standard elevated plus-maze and the time spent in the open arms and the ratio of open arm entries during 5 min, were measured. The data analyzed by using ANOVA and Tukey test.

 

Results: BBS in dose dependently manner increase which the anxiety reaction in mice. Animals had spent lower time and ratio of open arm entries in compare with control group significantly (P<0.05) and BBS only in dose of 1.25 µg/kg did not showed significantly effect.

 

Conclusion: This study indicated that Bombesin in dose dependently manner have important role in modulate anxiety reaction in EPM in mice.

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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 & Objective: The effects of acute and chronic exposures to opiate drugs on anxiety process are controversial. Acute morphine injection showed the beneficial effects on anxiety. Morphine withdrawal induced severe anxiety response in morphine dependence rats. Whereas, the effects of chronic administrations of morphine on anxiety process are less studied. Furthermore, this study was designed to assess the role of morphine dependence on the level of anxiety in Rat. Materials & Methods: In this experimental study, Twenty male Wistar rats (250-300 gr) were made dependent by chronic administration of morphine in drinking water that lasted at least 21 days. Control groups received only sucrose in their water. This study utilized the elevated plus- maze model to evaluate anxiogenic-like behavior in rats. Four fundamental behavior patterns were recorded for 5 minutes: the time spent on open arms, the number of entries into open arms, stretched-attend posture and defecation. Immediately after test, the locomotor activity of each animal was tested by using an automated activity monitor system. The data were analyzed by independent t-test and two-way analysis of variance (ANOVA). Results: Finding indicated that the time spent on open arms and the numbers of entries into open arms were significantly shorter in morphine dependence group than control group (P<0.05). Also, the numbers of stretched-attend posture and defecation were significantly higher in morphine group (P<0.05). Whereas, there were no significant differences between groups in locomotor activity. Conclusion: This study showed that dependent rats may rapidly predispose anxiogenic- like effects in stressful conditions and without the effect on motor activity.

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Background and Objective: Post-traumatic stress disorder (PTSD) is an anxiety, which is induced by exposure to life-threatening trauma and produces memory dysfunctions. This study was done to evaluate the effect of β-estradiol on traumatic memory after post-traumatic stress disorder induced by modified single-prolonged stress model in male rats. Materials and Methods: This experimental study was done on 70 male Wistar rats, weighted 200-250 grams. Initially 30 rats randomly allocated into control, shock and single prolonged stress accompanied shock (SPS&S). In SPS&S group immobilized for 2h, followed immediately with a 20 min forced swim conducted in a cylindrical filled with water. After recuperating for 15 min, animals anesthetized with ether. After 30 min recovery, stressed rats placed in the conditioned fear system (CFS). They received one 1mA, 4 second electric foot shock and remained in the chamber for another 60 second before being returned to their home cages. Shock group: Animals placed in CFS and only received the same shock as previous experiment. Naive group: Animals were removed from their home cages and exposed to chamber without receiving any foot shock. 1, 2 and 3 week later, animals in all groups were re-exposed to the shock chamber for 3 min, in order to examine conditioned fear response. In the second experiment rats were injected with β-estradiol (90 µg/kg), one and two week after training. Date were analyzed using SPSS-16, ANOVA and LSD tests. Results: SPS&S significantly induced freezing response (traumatic memory) compared with controls and shock groups (P<0.05) following three weeks. This response significantly reduced due to repetitive injection of β-estradiol in rats (P<0.05). After three weeks causes of enhanced freezing response (traumatic memory) compare with both, shock and sham groups (P<0.001). β-estradiol significantly reduced this response in rats (P<0.001). Conclusion: β-estradiol's administration following PTSD induction by modified single-prolonged stress, significantly decreased the freezing response. Therefore, β-estradiol can prevent the formation of traumatic memory.