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Background and purpose: Post-traumatic stress disorder (PTSD (is a psychotic illness caused by different types of stressors and is associated with high economic and psychological burdens on health systems. Physiological studies of the brain have shown that serum corticosterone and insulin-like growth factor 1 (IGF-1) levels have important roles during brain damage and trauma to the nervous system. In this project, we studied the effect of exercise as an effective factor on improving anxiety and serum levels of corticosterone and IGF-1in male PTSD rats.
Materials and methods: In this experimental study, single prolonged stress (SPS) was used to induce PTSD in male Wistar rats. The animals were divided into two groups: Sham (Non-SPS [NSPS]) and SPS. The two groups were then divided into two subgroups and one of the subgroups in each group did the exercise after two weeks which continued for four weeks according to the following program: moderate treadmill exercise, 5 days a week; the first two weeks 10m/min and the second two weeks 15m/min). Then, anxiety test was performed by open field test and serum levels of IGF-1 and corticosterone were measured using Eliza.
Results: The rats in SPS group exhibited increased anxiety levels in open field test, decreased serum IGF-1 levels, and increased serum corticosterone levels compared with the controls. Moderate treadmill exercise alleviated SPS-induced alterations, anxiety, and IGF-1 and corticosterone levels.
Conclusion: Moderate exercise could be used as a useful complementary treatment in behavioral and molecular injuries in PTSD patients.

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Background and purpose: Unpredictable stressors cause changes in behavioral parameters such as motor and exploratory behaviors, feeding, and sexual and anxiety behaviors. Stress leads to the release of corticosteroids and, as a result, causes dysfunction in different parts of the nervous system. A decrease in the synaptic levels of serotonin or norepinephrine in different parts of the brain such as the prefrontal cortex and a decrease in BDNF production in the hippocampus may also contribute to stress-related complications. Posttraumatic stress disorder occurs in some people after facing a severe stressful event. In PTSD, the activity and function of many physiological systems are disturbed. Fluoxetine, or Prozac, is used to treat neurological disorders such as depression and anxiety and inhibits the reuptake of serotonin by the serotonin transporter (SERT) in neurons. Some studies have shown that females respond better to SSRI antidepressants than males, which may be due to the interaction between estrogenic and serotonergic pathways. BDNF is a member of the neurotrophin family and is expressed in several tissues and cells such as the brain and blood. Its role in several mental disorders, such as depression, anxiety, eating disorders, and PTSD, has been identified. SPS (single prolonged stress) as an animal model of PTSD decreases the mRNA expression of BDNF in hippocampus rats and causes anxiety-like behaviors. The role of gender differences in the effect of antidepressants and clinical interventions in psychotic diseases is also discussed. Sex hormones in women affect the pharmacokinetics and efficacy of antidepressants. Women respond better to fluoxetine than men during reproductive years. Considering the different results regarding the effectiveness of effective drugs in the treatment of psychotic diseases in both sexes, in this study, we aim to investigate the response of male and female rats exposed to stress to the trial of fluoxetine.
Materials and methods: In this experimental study, Wistar male and female rats with an average weight of 200-250 grams were used (56 animals, 8 groups of 7). The selection of the number of animals was based on previous studies in this field. After the drug intervention period, and fear and anxiety suppression test, the animals were killed under deep anesthesia, and a blood sample was collected to prepare serum to measure BDNF and corticosterone levels (using the Eliza kit of Germany Zelbio Company and according to the kit protocol). All experiments were performed according to the laboratory animal protocol of Mazandaran University of Medical Sciences.
The work steps are as follows: 1. Creation of PTSD through SPS was done in three stages, 2. Drug intervention: the drug dose for all groups is 10 mg/kg/day for 4 weeks dissolved in drinking water, 3. Evaluation of anxiety-like behaviors with the light-dark box (L/D BOX), 4. Evaluation of the ability to forget painful memories with the fear silence test, 5. Measurement of BDNF and corticosterone in serum by Eliza method.
Results: In this study, it was observed that male and female rats that were exposed to single prolonged stress showed a decrease in fear extinction an increase in anxiety-like behaviors in the dark-light box test, and an increase in serum corticosterone. Fluoxetine led to an increase in the percentage of fear extinction, a decrease in the Entrance Latency in the light area, the Time in the Light Compartment, the number of rearing, and a decrease in serum corticosterone significantly in both sexes(P<0.05). The change in serum BDNF levels in both sexes before and after stress was not significant.
Conclusion: The results of the study showed that exposure to stress leads to behavioral and biochemical damage in male and female rats. The use of fluoxetine 10 mg/kg for 4 weeks improved the damage caused by stress, but there was a significant difference in Response of both genders to the above treatment was not observed.
 

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Background and purpose: Post-traumatic stress disorder (PTSD) is a psychiatric disorder caused by traumatic events. Various treatments, including pharmacotherapy and psychotherapy, have been investigated, but the role of exercise as a promising intervention remains underexplored. From a neurobiological perspective, PTSD is associated with dysregulation in several brain regions involved in emotion regulation, memory processing, and fear responses. This study investigates the effects of voluntary and forced exercise on behavioral responses and serum levels of IGF-1 and corticosterone in ovariectomized rats with PTSD.
Materials and methods: Fifty-six adult female Wistar rats were randomly selected and kept under normal laboratory conditions. First, the rats were divided into control and ovariectomized groups. Ovariectomy was performed under deep anesthesia. After a recovery period, the single prolonged stress (SPS) method was used to induce PTSD. Rats were subjected to voluntary exercise using a running wheel or forced exercise on a treadmill. Anxiety was measured using the elevated plus maze, and cognitive performance was assessed using the Object Recognition Memory Test. Afterward, the animals were euthanized under deep anesthesia, and serum samples were collected. Corticosterone and IGF-1 levels were measured by ELISA.
Results: In the control and ovariectomized groups, both types of exercise resulted in decreased anxiety, with a more pronounced anti-anxiety effect observed in the voluntary exercise group. Voluntary exercise significantly improved memory in both the control and ovariectomized groups. Forced exercise also enhanced memory in the ovariectomized group, albeit to a slightly lesser extent than voluntary exercise. Both types of exercise in the control and ovariectomized groups led to a significant reduction in serum corticosterone levels. Notably, this reduction was more pronounced with voluntary exercise compared to forced exercise.
Conclusion: Voluntary exercise effectively reduces anxiety, enhances cognitive function, and modulates physiological stress markers in ovariectomized rats with PTSD.