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  Background & objectives: Brain ischemia leads to irreversible functional and structural damage in various regions of the brain, especially in the hippocampus. There is an evidence indicating the physical exercise has neuroprotective effects and may decrease the cerebral ischemia/ reperfusion injury in rats. The purpose of this study was the study of the effect of exercise preconditioning on memory deficits and neuronal cell death in CA3 pyramidal cells of the rat hippocampus following transient global ischemia.

  Methods: 21 male rats weighing 260-300g were randomly selected and allocated into three groups (sham, ischemia and exercise+ischemia). The rats in exercise group were trained to run on a treadmill 5 days a week for 4 weeks. Ischemia induced by occlusion both common carotid arteries (CCA) for 20 minutes. The passive avoidance memory test using a Shuttle box used to assess the impairment of memory. The amount of cell death was measured using cresyl violet staining method.

  Results: The results showed that cerebral ischemia is associated with memory impairment, and physical activity before ischemia improves ischemia-induced memory impairments significantly (p<0.05). In addition, ischemia leads to cell death in hippocampal CA3 area neurons and exercise also reduces ischemia-induced cell death significantly (p<0.05).

  Conclusion: This study showed that exercise, when is used as a preconditioning stimulant , has a neuroprotective effects against brain ischemia.

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Background & objectives: Temporal lobe epilepsy is associated with neuronal apoptosis. Curcumin has antioxidant and anticonvulsant activities, therefore this study was conducted to assess involvement of Bax and Bcl2 in protective effect of curcumin in epileptic rats.

Methods: 28 rats were divided into sham, curcumin-pretreated sham, epileptic (kainate), and curcumin-pretreated epileptic groups. Experimental model of epilepsy was induced by intrahippocampal administration of kainic acid. Rats received curcumin at a dose of 100 mg/kg. Finally, Nissl staining and Bax and Bcl2 immunohistochemistry were conducted on hippocampal sections and data were analyzed using one-way ANOVA and unpaired t-test. The p-value less than 0.05was considered statistically significant.

Results: Induction of epilepsy was followed by a significant seizure and curcumin pretreatment significantly reduced seizure intensity (p<0.01). In addition, there were no significant differences between the groups in Nissl staining of CA3 area neurons. In addition, Bax positive neurons were observed in CA3 area in kainate group and significantly decreased in curcumin pretreated rats (p<0.05). Meanwhile, Bcl2 positive neurons were also moderately observed in kainate group and curcumin pretreatment significantly increased it (p<0.05).

Conclusion: Curcumin pretreatment exhibits anticonvulsant activity in epileptic rats. It also decreases the expression of pro-apoptotic protein Bax and significantly enhances the expression of anti-apoptotic protein Bcl2 and hence could reduce neuronal apoptosis.

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Background & objectives: Depression is a common and debilitating brain disorder and a type of psychiatric syndromes. The most common symptoms of this disease are irritability, worthlessness, sleep problems and anxiety disorders. Reserpine is a drug that can cause depression in animals if used at a very low dose. Electroconvulsive therapy (ECT) is one of the most effective non-pharmacological treatments for depression. In this study, the effect of electroconvulsive therapy on male rats depressed by reserpine in behavioral tests and neural counting in the hippocampus and prefrontal cortex areas was investigated.
Methods: In this experimental study, 40 male rats were used and they were divided into four groups of ten: 1-control group, 2- ECT group, 3- Depressed group induced by reserpine (0.2 mg/kg i.p.), 4- Depressed + ECT group. Open field, sucrose preference, forced swimming and elevated plus maze tests were used to evaluate anxiety and depression-related behavioral function. At the end of the tests, histochemical studies were performed with neuronal counting in the hippocampus and prefrontal cortex.
Results: The results of anxiety and depression behavioral tests showed a significant difference between depressed group and depressed+ECT group (p<0.05). Similarly, studies of the tissue degeneration from hippocampal and prefrontal incisions, showed that ECT could significantly decrease cell death in the depressed+ECT group compared to the depressed group (p<0.05).
Conclusion: According to the results, ECT can reduce the anxiety and depression behaviors induced by reserpine injections in depressed animals and can cause neurogenesis in the hippocampus and prefrontal cortex.

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Background & objectives: Exercise, with beneficial effects on brain health and cognitive function reduces the destructive effects of some neurological diseases such as Alzheimer's. The aim of this study was to evaluate the effect of four weeks of aerobic exercise on cognitive function and expression of Sirt1, CREB and BDNF genes in the hippocampus of male Wistar rats with Alzheimer's disease.
Methods: The statistical population included 18 male Wistar rats from the Pasteur Institute. Rats were randomly divided into three groups including Alzheimer's group, Alzheimer's disease-exercise group and a healthy control group. Alzheimer's disease group was induced by injecting Aβ42 into the hippocampus. Seven days after surgery, the rats performed the aerobic exercise for four weeks (five sessions per week at a speed of 10-15 m/min). They underwent behavioral tests 48 hours after the last training session. Twenty four hours later, rat hippocampal tissue was extracted. Sirt1, CREB and BDNF mRNAs were measured using Real time-PCR.
Results: Learning and spatial memory performance decreased in rats of Alzheimer's disease group compared to a healthy control group (p˂0.001). Decreased mRNA expression of Sirt1, CREB and BDNF genes was observed in the hippocampal tissue of Alzheimer's disease group compared with the healthy control group (p˂0.001). Alzheimer's rats with intermittent aerobic exercise had improved learning function, spatial memory and increased mRNA expression levels of Sirt1, CREB and BDNF genes in comparison with Alzheimer's disease group (p˂0.001).
Conclusions: Periodic aerobic exercise in rats with Alzheimer's disease can improve spatial learning and memory by positively regulating the Sirt1/ CREB/ BDNF signaling pathway in hippocampal tissue.

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Background & objectives: The deposition of amyloid beta (Aβ) peptide in the brain is one of the most important features of Alzheimer's disease. In addition to memory loss, Aβ can lead to depression behavior. Alpha-pinene is a type of monoterpene that has antioxidant, anti-inflammatory, and neuroprotective effects. Here, by using an animal model for Alzheimer's disease, we investigated the effect of alpha-pinene on neuronal cell death in the hippocampus and depression induced by Aβ_1-42.
Methods: Male Wistar rats weighing 240-260 g were divided into four groups including control, alpha-pinene, Aβ, and Aβ-alpha-pinene. Rats were placed in stereotaxic surgery apparatus and Aβ_1-42 was injected into the hippocampus (4 µg per side) and alpha-pinene was treated intraperitoneally (50 mg/kg) for 14 consecutive days. At the end of the course, the level of depression was assessed using the forced swimming test. The animals' hippocampus was also examined microscopically after Nissl staining.
Results: Intra-hippocampal injection of Aβ_1-42 increased the total immobility time in the forced swimming test (p<0.01), decreased the number of pyramidal neurons in the CA1 area (p<0.001), and reduced the thickness of the neuronal layer in this region of ​​the hippocampus. Treatment with alpha-pinene largely prevented these changes.
Conclusion: It can be concluded that alpha-pinene decreased the beta-amyloid-induced depressive behavior in rats and inhibited the neuronal loss, suggesting that this neuroprotective compound may have a critical role in depression. Alpha-pinene is probably a suitable therapeutic strategy for repressing Aβ-induced neurodegeneration

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Background & objectives: Brain trauma is one of the most common causes of damage to the central nervous system which can lead to death and long-term disability. The present study aimed at investigating the effect of 8 weeks of swimming exercise on the level of memory and interleukin 10 (IL-10) in the hippocampus and prefrontal cortex of mice with brain trauma.
Methods: 40 male NMRI mice were randomly divided into four groups (control, swimming, trauma, swimming + trauma). After completing the exercise protocol, induction of trauma was performed by the weight -drop method. Ten days after trauma induction, the mice were evaluated for spatial memory with Y-maze test. The IL- 10 level was measured using ELISA technique. One-way analysis of variance and Tukey post hoc test were used for statistical analysis at a significance level of p<0.05 and using SPSS software version 26.
Results: The study results indicated that eight weeks of swimming exercise significantly increase memory in mice with brain trauma (p=0.001). Furthermore, eight weeks of swimming exercise significantly increase the level of IL-10 in the hippocampus of mice with brain trauma (p=0.001). However, this increase was not significant in the prefrontal cortex (p=0.126).
Conclusion: The results of the present study showed that swimming exercise before induction of brain trauma reduces inflammation and memory disorders and facilitates recovery after injury. Previous exercise training can probably reduce inflammation by increasing the amount of anti-inflammatory cytokines, including interleukin-10, and limit secondary damage with its protective effect.