:: Volume 6, Issue 4 (Autumn - 2018) ::
Shefaye Khatam 2018, 6(4): 5-13 Back to browse issues page
The Effect of Gallic Acid on Motor Learning and Cerebellar Level of Brain Derived Neurotrophic Factor in a Rat Model of Autism
Mohammad Amin Edalatmanesh * , Parvin Samimi
Department of Physiology, College of Sciences, Shiraz Branch, Islamic Azad University, Shiraz, Iran , amin.edalatmanesh@gmail.com
Abstract:   (7529 Views)
Introduction: Exposure to Valproic acid (VPA) during pregnancy in rats leads to oxidative stress, brain deficits, and autistic-like behaviors in the offspring. On the other hand, Gallic acid (GA) can effectively be used in the treatment of free radicals-induced nervous system disorders. The aim of this study was to investigate the effect of GA on motor learning and cerebellar level of brain derived neurotrophic factor (BDNF) in rats embryonically exposed to VPA. Materials and Methods: Pups of 30 pregnant rats were randomly divided into 5 groups: control, VPA (500 mg/kg Valproic acid) at embryonic day (ED) 12.5 groups as well as three groups of VPA+GA50, VPA+GA100, and VPA+ GA200 (receiving 50, 100 and 200 mg/kg GA, respectively). GA was orally administered from 12 to 19 ED. Then, to assess the motor disorders beam walking and rotarod tests were carried out at postnatal day 30. Finally, the cerebellar level of BDNF was measured using ELISA. Results: Impairments were observed in the motor function test of the VPA group compared to the control rats. In contrast, GA-treated groups have a significant improvement in speed on beam and balance in beam walking test as well as an increase time spent in rotarodas well. A significant increase of BDNF was seen in GA-treated rats compared to VPA group. Conclusion: GA can alleviate the adverse effects of VPA on motor learning and balance in a rat model of autism.
Keywords: Gallic Acid, Valproic Acid, Motor Disorders, Autistic Disorder, Rats
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Type of Study: Research --- Open Access, CC-BY-NC | Subject: Basic research in Neuroscience
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Volume 6, Issue 4 (Autumn - 2018) Back to browse issues page