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Showing 8 results for Brain-Derived Neurotrophic Factor

Marzieh Moghadas, Mohammad Amin Edalatmanesh, Mahmoud Hosseini,
Volume 2, Issue 4 (12-2014)
Abstract

Introduction: Pathophysiology of depression is a controversial issue. Hippocampal lesions could lead into depression as well as to changing the levels of several cytokines, including brain-derived neurotrophic factor (BDNF) and tumor necrosis factor alpha (TNF- α). The present study was aimed to investigate the mechanism of depression induced by trimethyltin (TMT) intoxication and to study the effect chronic administration of lithium chloride (Li) on depression in this animal model. Materials and Methods: The animals were divided into TMT+Li20, TMT+Li40, TMT+ Li80 and TMT+Salin groups, which were received 8 mg/kg TMT and 20, 40 or 80 mg/kg of Li or saline, respectively, for fourteen days. In order to define the depression level, the immobility time of the rats was measured in the forced swim test (FST), and tail suspension test (TST). Then, the serum level of TNF-α, BDNF and wet weight of the brains were measured. Results: The immobility time in FST and TST was longer in the rats who received TMT, whereas the rats receiving Li showed a significantly less immobility compared to the TMT+Saline group. In addition, Li administration increased the serum level of BDNF and wet weight of the brains and decreased the TNF-α level compared to the TMT+Saline group. Conclusion: The decrease in BDNF or the increase in inflammation factors (especially TNF-α) occurred in accompany by depression symptoms in TMT intoxication model. On the other hand, chronic administration of Li may modulate the cytokines and amelioration of behavioral symptoms.


Marzieh Moghadas, Mohammad Amin Edalatmanesh,
Volume 3, Issue 2 (6-2015)
Abstract

Introduction: Trimethyltin (TMT) is an organotin neurotoxicant which causes selective degeneration in central nervous system such as hippocampus. TMT intoxication is the cause of mood-cognitive and motor deficits in human and rodents. The present study aimed to investigate the effect of lithium chloride (LiCl) on brain derived neurotrophic factor (BDNF) level in the hippocampus and anxiety-exploratory behaviors in TMT intoxication rat model. Materials and Methods: In order to induce intoxication, TMT (8 mg/kg) was injected intraperitoneally to the rats. The test groups (TMT+Li) received 0.5, 1 and 1.5 meq/kg of LiCl respectively and the TMT+Saline group received normal saline for 14 days after TMT intoxication. The elevated plus maze, dark-light box and open field tests were conducted in order to investigate the anxiety symptoms and exploratory behaviors. Then, the hippocampal level of BDNF was measured using ELISA. Results: The findings indicated an increase in anxiety behaviors and a decrease in exploratory ones. In addition, the hippocampal level of BDNF was decreased in the TMT-treated rats. However, LiCl treatment revealed significant effects on decreasing the anxiety level with exploratory behaviors modification in the behavioral tests. Conclusion: LiCl, having sufficient neuroprotective effects, can be used as a solution to manage the anxiety symptoms and cognition deficits after TMT intoxication.


Samaneh Rafiei, Yunes Bazyar, Mohammad Amin Edalatmanesh,
Volume 4, Issue 1 (3-2016)
Abstract

Introduction: The aim of this study was to investigate the effect of gallic acid on hippocampal level of brain derivative neurotrophic factor (BDNF) in trimethyltin chloride (TMT)- intoxication rats after eight weeks of endurance training. Materials and Methods: Seventy Sprague-dawley male rats were selected and randomly divided into seven groups, including: (1) Control, (2) Sham, (3) Gallic acid 50, (4) Gallic acid 100, (5) Endurance training (4), (6) Training + Gallic acid 50, and (7) Training + Gallic acid 100. Hippocampal degeneration was induced by TMT (8 mg/kg) in all groups except control animals. During eight weeks, rats of groups 3, 6 and 7 ran on treadmill’s without incline at a speed of 15 to 20 meters per minute for 15 to 30 minutes per session, five times weekly. In addition, groups 4 and 6 were treated with gallic acid (50 mg/kg) and groups 5 and 7 with gallic acid (100 mg/kg) every day for 14 days. Results: The findings showed that hippocampal levels of BDNF in all test groups was significantly higher than sham group. Conclusion: Endurance training and gallic acid as well as the combination of them increase the level of hippocampal BDNF in a model of TMT-intoxication.


Hossein Nazari, Sajad Heydarpoor, Abuzar Mohamadi Mofrad, Yazgaldi Nazari, Araz Nazari,
Volume 4, Issue 2 (6-2016)
Abstract

Introduction: The aim of this study was to investigate the effect of consuming vitamin C on the serum level of Brain-derived neurotrophic factor (BDNF) among healthy inactive young men. Materials and Methods: In this semi-empirical study, 18 healthy inactive men were randomly divided into two groups; a group consuming vitamin C as a supplement and a control group. Subjects in consuming vitamin C group received 500 milligrams of vitamin C supplement daily for one week. The control group consumed placebo. Blood samples of participants were taken in fasting mode to measure BDNF concentration. BDNF was measured by ELISA method. Results: The serum levels of BDNF significantly increased one week after receiving vitamin C compared to the control group. In addition, the level of BDNF in subjects received vitamin C for one week significantly increased compared to the beginning of the investigation. Conclusion: Data indicate that consuming vitamin C increased the serum concentration of BDNF in healthy inactive men.


Maryam Borhani-Haghighi, Fatemeh Alipour, Parastoo Barati,
Volume 4, Issue 3 (12-2016)
Abstract

Post-traumatic stress disorder (PTSD) is a syndrome causing from a severe traumatic happening that leads to threatened death or injury. PTSD is associated with changes in limbic, hippocampal, and prefrontal cortical region function due to changes in synaptogenesis, dendritic modifying, and neurogenesis. Changes in neuron in PTSD patients result from pathophysiological disturbances in inflammatory, metabolic, and apoptic processes. Brain-derived neurotropic factor (BDNF) is a neurotrophin that functions as survivorship factor for selected neurons of central nervous system and it can regulate synaptic plasticity, memory processes and behavior in the limbic system. Failure to produce BDNF in the brain can lead to a variety of central nervous system disorders. Researches indicate that impairment in the regulation of neural BDNF occurs in conditions of PTSD. It is found that level of BDNF in serums of PTSD patients were lower as compared to related controls. It is suggested that BDNF may be involved in pathophysiology of PTSD and enhancing BDNF-related signaling and restoring level of BDNF in serum may be considered as consequently therapeutic.


Abolfazl Shayan Nooshabadi, Alireza Saberi Kakhki, Mehdi Sohrabi, Mohamad Ali Dowlati,
Volume 4, Issue 4 (12-2016)
Abstract

Introduction: Brain-derived neurotrophic factors (BDNF) play a role on induction and maintenance of memory and learning. The BDNF gene Val66Met polymorphism impairs expression of this protein. Due to difference between the neural principles operating during motor memory consolidation and the neural principles operating during practice (acquisition) and the effect of BDNF on both of these processes, the aim of the study was to study the effect of val66met polymorphism on acquisition and motor memory consolidation in the process of learning of throwing motor skill. Materials and Methods: We randomly selected one hundred university students of Kashan , Iran (mean age: 21.6±2.2 years). After blood sampling, extraction of genomic DNA, implementation of polymerase chain reaction, analyzing of PCR by 1.5 percent Electrophoresis Gel, and in the end sequencing by ABI PRISM 7000 Sequencing Analyzer, 46 participants were identified without val66met polymorphism, and 54 participants identified affected by the polymorphism (met-carriers). 10 participants of each genetic group (20 people) after pre-test practiced backhand baseball pitch for six sessions. After 48 and 96 hours they participated in two consecutive retention tests. Results: Our data showed no difference between met-carriers and people without the polymorphism in acquisition and the first retention test. However, met-carriers were significantly weaker than people without the polymorphism in the second retention test. Conclusion: These findings suggest that the BDNF val66met polymorphism has higher impact on motor learning in the consolidation phase than acquisition phase.


Omid Reza Salehi, Seyed Ali Hoseini,
Volume 5, Issue 2 (4-2017)
Abstract

Introduction: Diabetes mellitus is a metabolic disease which can induce neuropathy, retinopathy and nephropathy. Exercises have a major role in reduction of these complications. Data on the role of exercises on BDNF and insulin levels in diabetic patients are controversial and there is no suitable exercise program for improvement of these indexes in diabetic patients. The aim of the present study was to investigate the effect of endurance trainings on BDNF and insulin levels in diabetic rats. Materials and Methods: 32 diabetic rats were divided in 4 groups of 8 rats; (1) diabetic rats sacrifice at first week, (2) diabetic rats sacrifice at last week, (3) diabetic rats with moderate intensity endurance training and (4) diabetic rats with high intensity endurance training. In addition, 16 healthy rats were divided in 2 groups of healthy sacrifice at first week and healthy sacrifice at last week. Rats of groups 3 and 4 ran on treadmill for 8 weeks (3 sessions per week, 60 minutes per session with intensity of 10- 17 and 17- 28 meter per minute). Results: Induction of diabetes by streptozotocin significantly reduced BDNF and insulin levels in rats. Eight weeks’ moderate and high intensity endurance training significantly increased BDNF level but had no effect on insulin values in diabetic rats. Conclusion: Moderate and high intensity endurance training may have protective effect on diabetes–induced complications in diabetic rats.


Seyed Damoon Sadoughi, Jina Khayatzadeh,
Volume 6, Issue 1 (1-2018)
Abstract

Introduction: Alzheimer's disease (AD) is a progressive neurodegenerative disease of the central nervous system. Neuronal injury and oxidative stress in AD increases the level of inflammatory cytokines. Curcumin has antioxidant and neuroprotective properties. The aim of this study was to determine the effect of curcumin on hippocampal levels of brain-derived neurotrophic factor (BDNF) and serum levels of inflammatory cytokines in an experimental model of AD. Materials and Methods: 28 male rats divided into 4  groups: Control group (30 days, intraperitoneal injection of DMSO), AD control group (30 days, intraperitoneal injection of DMSO, after induction of AD) and two AD treatment groups with application of 50 and 100 mg/kg of curcumin (30 days, intraperitoneal injection of curcumin, after induction of AD). AD was induced by intraperitoneal injection of 8 mg/kg trimethyltin chloride. At the end of the treatment period, the hippocampal levels of BDNF and serum levels of different cytokines (TNF-α, IL-1β and IL-6) were measured by ELISA method. Results: Compared to AD control group, administration of curcumin with dose of 100 mg/kg significantly increased the hippocampal levels of BDNF (P=0.002) and decreased the serum levels of TNF-α, IL-1β and IL-6 (P=0.001). Conclusion: Administration of curcumin may decrease the serum levels of inflammatory cytokines in AD, possibly via enhancement of the hippocampal levels of BDNF.  This study suggests the protective effect of curcumin against neuronal damages and oxidative stress in AD.



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مجله علوم اعصاب شفای خاتم The Neuroscience Journal of Shefaye Khatam
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