Tehran University of Medical Sciences

Science Communicator Platform

Stay connected! Follow us on X network (Twitter):
Share this content! On (X network) By
Neuronal Injury and Death Following Focal Mild Brain Injury: The Role of Network Excitability and Seizure Publisher



Ghadiri T1, 2 ; Gorji A2, 3, 4 ; Vakilzadeh G2 ; Hajali V5 ; Khodagholi F6 ; Sharifzadeh M7
Authors
Show Affiliations
Authors Affiliations
  1. 1. Department of Neuroscience, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, 29 Bahman Blvd, East Azarbayjan, Tabriz, Iran
  2. 2. Shefa Neuroscience Research Center, Khatamolanbia Hospital, Tehran, Iran
  3. 3. Department of Neurosurgery, Department of Neurology, Epilepsy Research Center, Munster University, Munster, Germany
  4. 4. Razavi Neuroscience Center, Razavi Hospital, Mashhad, Iran
  5. 5. Quchan Higher Health Education Center, Mashhad University of Medical Sciences, Mashhad, Iran
  6. 6. Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran
  7. 7. Faculty of Pharmacy, Department of Toxicology, Tehran University of Medical Sciences, Tehran, Iran

Source: Iranian Journal of Basic Medical Sciences Published:2020


Abstract

Objective(s): While traumatic brain injury (TBI) is a predisposing factor for development of posttraumatic epilepsy (PTE), the occurrence of seizures following brain trauma can infuriate adverse consequences of brain injury. However, the effect of seizures in epileptogenesis after mild TBI cannot yet be accurately confirmed. This study was designed to investigate the histopathological and molecular modifications induced by seizures on traumatized brain. Materials and Methods: Using a new method, head was traumatized and seizures were evoked by subconvulsive dose of pentylenetetrazole (PTZ) fifteen days after induction of focal mild TBI. Convulsion assessments were performed one hour after PTZ injection and was followed by histopathological and molecular evaluations. Results: A significantly higher score and longer duration of seizure attacks as well as higher number of epileptiform discharges were observed in the TBI+PTZ group compared to sham and TBI groups. An elevated number of apoptotic cells was observed in the TBI+PTZ group compared to sham and TBI rats. Molecular investigations revealed higher levels of Bax/Bcl2 ratio, Caspase 3, and NF-κB in the TBI+PTZ group compared to the other animal groups. The value of Nrf2 did not change after mild TBI compared to sham and PTZ control groups. Occurrence of seizures after TBI, however, significantly decreased the level of Nrf2. Conclusion: Our data indicated that seizure occurrence following mild TBI aggravates cell injury and death via activation of neuroinflammatory processes and may increase the risk of PTE. Additionally, our results suggest a potential protective role of Nrf2 after chemically evoked PTE. © 2020 Mashhad University of Medical Sciences. All rights reserved.
Related Docs
1. The Effect of Melatonin on Behavioral, Molecular, and Histopathological Changes in Cuprizone Model of Demyelination, Molecular Neurobiology (2016)
2. Cognitive Impairments and Neuronal Injury in Different Brain Regions of a Genetic Rat Model of Absence Epilepsy, Neuroscience (2015)
3. A Camp Analog Attenuates Beta-Amyloid (1–42)-Induced Mitochondrial Dysfunction and Spatial Learning and Memory Deficits, Brain Research Bulletin (2018)
Experts (# of related papers)
View all Related Experts
Mohammad Sharifzadeh (2)
Maryam Jafarian (1)