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MRI changes and complement activation correlate with epileptogenicity in a mouse model of temporal lobe epilepsy

The complex pathogenesis of temporal lobe epilepsy includes neuronal and glial pathology, synaptic reorganization, and an immune response. However, the spatio-temporal pattern of structural changes in the brain that provide a substrate for seizure generation and modulate the seizure phenotype is yet... Full description

Journal Title: Brain Structure and Function 2014, Vol.219(2), pp.683-706
Main Author: Kharatishvili, Irina
Other Authors: Shan, Zuyao , She, David , Foong, Samuel , Kurniawan, Nyoman , Reutens, David
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 1863-2653 ; E-ISSN: 1863-2661 ; DOI: 10.1007/s00429-013-0528-4
Link: http://dx.doi.org/10.1007/s00429-013-0528-4
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recordid: springer_jour10.1007/s00429-013-0528-4
title: MRI changes and complement activation correlate with epileptogenicity in a mouse model of temporal lobe epilepsy
format: Article
creator:
  • Kharatishvili, Irina
  • Shan, Zuyao
  • She, David
  • Foong, Samuel
  • Kurniawan, Nyoman
  • Reutens, David
subjects:
  • Epileptogenesis
  • Spontaneous recurrent seizures
  • Temporal lobe epilepsy
  • Magnetic resonance imaging
  • Complement
  • Hippocampus
  • Parahippocampal cortex
  • Epilepsy animal models
ispartof: Brain Structure and Function, 2014, Vol.219(2), pp.683-706
description: The complex pathogenesis of temporal lobe epilepsy includes neuronal and glial pathology, synaptic reorganization, and an immune response. However, the spatio-temporal pattern of structural changes in the brain that provide a substrate for seizure generation and modulate the seizure phenotype is yet to be completely elucidated. We used quantitative magnetic resonance imaging (MRI) to study structural changes triggered by status epilepticus (SE) and their association with epileptogenesis and with activation of complement component 3 (C3). SE was induced by injection of pilocarpine in CD1 mice. Quantitative diffusion-weighted imaging and T2 relaxometry was performed using a 16.4-Tesla MRI scanner at 3 h and 1, 2, 7, 14, 28, 35, and 49 days post-SE. Following longitudinal MRI examinations, spontaneous recurrent seizures and interictal spikes were quantified using continuous video-EEG monitoring. Immunohistochemical analysis of C3 expression was performed at 48 h, 7 days, and 4 months post-SE. MRI changes were dynamic, reflecting different outcomes in relation to the development of epilepsy. Apparent diffusion coefficient changes in the hippocampus at 7 days post-SE correlated with the severity of the evolving epilepsy. C3 activation was found in all stages of epileptogenesis within the areas with significant MRI changes and correlated with the severity of epileptic condition.
language: eng
source:
identifier: ISSN: 1863-2653 ; E-ISSN: 1863-2661 ; DOI: 10.1007/s00429-013-0528-4
fulltext: fulltext
issn:
  • 1863-2661
  • 18632661
  • 1863-2653
  • 18632653
url: Link


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titleMRI changes and complement activation correlate with epileptogenicity in a mouse model of temporal lobe epilepsy
creatorKharatishvili, Irina ; Shan, Zuyao ; She, David ; Foong, Samuel ; Kurniawan, Nyoman ; Reutens, David
ispartofBrain Structure and Function, 2014, Vol.219(2), pp.683-706
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subjectEpileptogenesis ; Spontaneous recurrent seizures ; Temporal lobe epilepsy ; Magnetic resonance imaging ; Complement ; Hippocampus ; Parahippocampal cortex ; Epilepsy animal models
descriptionThe complex pathogenesis of temporal lobe epilepsy includes neuronal and glial pathology, synaptic reorganization, and an immune response. However, the spatio-temporal pattern of structural changes in the brain that provide a substrate for seizure generation and modulate the seizure phenotype is yet to be completely elucidated. We used quantitative magnetic resonance imaging (MRI) to study structural changes triggered by status epilepticus (SE) and their association with epileptogenesis and with activation of complement component 3 (C3). SE was induced by injection of pilocarpine in CD1 mice. Quantitative diffusion-weighted imaging and T2 relaxometry was performed using a 16.4-Tesla MRI scanner at 3 h and 1, 2, 7, 14, 28, 35, and 49 days post-SE. Following longitudinal MRI examinations, spontaneous recurrent seizures and interictal spikes were quantified using continuous video-EEG monitoring. Immunohistochemical analysis of C3 expression was performed at 48 h, 7 days, and 4 months post-SE. MRI changes were dynamic, reflecting different outcomes in relation to the development of epilepsy. Apparent diffusion coefficient changes in the hippocampus at 7 days post-SE correlated with the severity of the evolving epilepsy. C3 activation was found in all stages of epileptogenesis within the areas with significant MRI changes and correlated with the severity of epileptic condition.
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abstractThe complex pathogenesis of temporal lobe epilepsy includes neuronal and glial pathology, synaptic reorganization, and an immune response. However, the spatio-temporal pattern of structural changes in the brain that provide a substrate for seizure generation and modulate the seizure phenotype is yet to be completely elucidated. We used quantitative magnetic resonance imaging (MRI) to study structural changes triggered by status epilepticus (SE) and their association with epileptogenesis and with activation of complement component 3 (C3). SE was induced by injection of pilocarpine in CD1 mice. Quantitative diffusion-weighted imaging and T2 relaxometry was performed using a 16.4-Tesla MRI scanner at 3 h and 1, 2, 7, 14, 28, 35, and 49 days post-SE. Following longitudinal MRI examinations, spontaneous recurrent seizures and interictal spikes were quantified using continuous video-EEG monitoring. Immunohistochemical analysis of C3 expression was performed at 48 h, 7 days, and 4 months post-SE. MRI changes were dynamic, reflecting different outcomes in relation to the development of epilepsy. Apparent diffusion coefficient changes in the hippocampus at 7 days post-SE correlated with the severity of the evolving epilepsy. C3 activation was found in all stages of epileptogenesis within the areas with significant MRI changes and correlated with the severity of epileptic condition.
copBerlin/Heidelberg
pubSpringer Berlin Heidelberg
doi10.1007/s00429-013-0528-4
pages683-706
date2014-03