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Brain Derived Neurotrophic Factor Modification of Epileptiform Burst Discharges in a Temporal Lobe Epilepsy Model



Eftekhari S1, 2 ; Mehrabi S3 ; Karimzadeh F1 ; Joghataei MT1, 2, 4 ; Khaksarian M5 ; Hadjighassem MR6, 7 ; Katebi M8 ; Soleimani M1, 4
Authors
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Authors Affiliations
  1. 1. Cellular and Molecular Research Center, Iran University of Medical Sciences, Tehran, Iran
  2. 2. Department of Neuroscience, School of Advanced Technologies in Medicine, Iran University of Medical Sciences, Tehran, Iran
  3. 3. Shefa Neuroscience Center, Khatam-Alanbia Hospital, Tehran, Iran
  4. 4. Department of Anatomy, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
  5. 5. Department of Physiology, School of Medicine, Lorestan University of Medical Sciences, Khorramabad, Iran
  6. 6. Department of Neuroscience, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran
  7. 7. Brain and Spinal Cord Injury Research Centre, Imam Khomeini Hospital, Tehran University of Medical Sciences, Tehran, Iran
  8. 8. Department of Anatomy, School of Medicine, Hormozgan University of Medical Sciences, Bandar Abbas, Iran

Source: Basic and Clinical Neuroscience Published:2016

Abstract

Introduction: Transforming Growth Factor-Beta 1 (TGF-β1) is a pleiotropic cytokine with potent anti-inflammatory property, which has been considered as an essential risk factor in the inflammatory process of Ischemic Stroke (IS), by involving in the pathophysiological progression of hypertension, atherosclerosis, and lipid metabolisms. -509C/T TGF-β1 gene polymorphism has been found to be associated with the risk of IS. The aim of this meta-analysis was to provide a relatively comprehensive account of the relation between -509C/T gene polymorphisms of TGF-β1 and susceptibility to IS. Methods: Male Wistar rats were divided into sham (receiving phosphate buffered saline within dorsal hippocampus), pilocarpine (epileptic model of TLE), single injection BDNF (epileptic rats which received single high dose of BDBF within dorsal hippocampus), and multiple injections BDNF (epileptic rats which received BDNF in days 10, 11, 12, and 13 after induction of TLE) groups. Their electrocorticogram was recorded and amplitude, frequency, and duration of spikes were evaluated. Results: Amplitude and frequency of epileptiform burst discharges were significantly decreased in animals treated with BDNF compared to pilocarpine group. Conclusion: Our findings suggested that BDNF may modulate the epileptic activity in the animal model of TLE. In addition, it may have therapeutic effect for epilepsy. More studies are necessary to clarify the exact mechanisms of BDNF effects.