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Traumatic Brain Injury Accelerates Kindling Epileptogenesis in Rats Publisher Pubmed



Eslami M1, 2, 3 ; Ghanbari E1 ; Sayyah M1 ; Etemadi F1 ; Choopani S1 ; Soleimani M4 ; Amiri Z5 ; Hadjighassem M6
Authors
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Authors Affiliations
  1. 1. Department of Physiology and Pharmacology, Pasteur Institute of Iran, Tehran, Iran
  2. 2. Department of Physiology, Paramedical Faculty, Shaheed Beheshti University of Medical Sciences, Tehran, Iran
  3. 3. Department of Neuroscience, School of Advanced Technology in Medicine, Tehran, Iran
  4. 4. Cellular and Molecular Research Center, Iran University of Medical Sciences, Tehran, Iran
  5. 5. Department of Basic Sciences, Faculty of Nutrition Sciences and Food Technology, Shaheed Beheshti University of Medical sciences, Tehran, Iran
  6. 6. Department of Neuroscience, School of Advanced Technology in Medicine, Tehran University of Medical Sciences, Tehran, Iran

Source: Neurological Research Published:2016


Abstract

Objectives: Traumatic brain injury (TBI) is a well-known cause of symptomatic epilepsy. In animal models of post-traumatic epilepsy (PTE), progression of trauma to epilepsy takes several weeks to months. Although this long process is similar to clinical PTE, it is costly and laborious. We used a combination of TBI and kindling as an accelerated animal model to develop epilepsy in much shorter period compared to that occurring in PTE. Methods: Traumatic brain injury was exerted to parieto-temporal cortex of anaesthetised rats by controlled cortical impact (CCI, 5 mm round tip, 4.5 mm/seconds velocity and 150 ms duration). Chemical kindling started 24 hours after CCI by intraperitoneal injection of 30 mg/kg pentylenetetrazole (PTZ) every other day until manifestation of three consecutive generalised seizures. Rapid electrical kindling of the amygdala began 1 week after TBI by exertion of 12 daily threshold stimuli (50 Hz mono-phasic square-wave stimulus of 1 ms per wave for 3 seconds) with 5 minutes interval between each stimulation until the rats became kindled. Results: Controlled cortical impact injury accelerated rate of both chemical and electrical kindling. Number of PTZ injections required for acquisition of generalised seizures decreased from 13.1 ± 1.6 in sham-operated animals to 7.1 ± 0.3 in traumatic rats (p < 0.05). The required number of stimuli to elicit electrically kindled focal and generalised seizures decreased from 24.0 ± 3.9 and 80 ± 6.5 in sham-operated animals to 6.6 ± 0.9 and 53 ± 6.5 in traumatic rats (p < 0.01), respectively. Limitations: Unlike the animal models of PTE in which recurrent seizures occur spontaneously after TBI, in our study, epilepsy is elicited by kindling stimulations. Discussion: Traumatic brain injury facilitates acquisition of epilepsy in both chemical and electrical kindling models. Combination of trauma and kindling can be considered as an inexpensive and time-saving animal model in PTE studies. © 2016 Informa UK Limited, trading as Taylor & Francis Group.