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

Byline: Irina Kharatishvili (1), Zuyao Y. Shan (1), David T. She (1), Samuel Foong (1), Nyoman D. Kurniawan (1), David C. Reutens (1,2) Keywords: Epileptogenesis; Spontaneous recurrent seizures; Temporal lobe epilepsy; Magnetic resonance imaging; Complement; Hippocampus; Parahippocampal cortex; Epil... Full description

Journal Title: Brain Structure and Function March, 2014, Vol.219(2), p.683(24)
Main Author: Kharatishvili, Irina
Other Authors: Shan, Zuyao Y. , She, David T. , Foong, Samuel , Kurniawan, Nyoman D. , Reutens, David C.
Format: Electronic Article Electronic Article
Language: English
Subjects:
Quelle: Cengage Learning, Inc.
ID: ISSN: 1863-2653
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recordid: gale_ofa359694248
title: MRI changes and complement activation correlate with epileptogenicity in a mouse model of temporal lobe epilepsy.(Report)
format: Article
creator:
  • Kharatishvili, Irina
  • Shan, Zuyao Y.
  • She, David T.
  • Foong, Samuel
  • Kurniawan, Nyoman D.
  • Reutens, David C.
subjects:
  • Seizures (Medicine)
  • Magnetic Resonance Imaging
  • Temporal Lobe Epilepsy
ispartof: Brain Structure and Function, March, 2014, Vol.219(2), p.683(24)
description: Byline: Irina Kharatishvili (1), Zuyao Y. Shan (1), David T. She (1), Samuel Foong (1), Nyoman D. Kurniawan (1), David C. Reutens (1,2) Keywords: Epileptogenesis; Spontaneous recurrent seizures; Temporal lobe epilepsy; Magnetic resonance imaging; Complement; Hippocampus; Parahippocampal cortex; Epilepsy animal models Abstract: 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. Author Affiliation: (1) Centre for Advanced Imaging, The University of Queensland, St Lucia, QLD, 4072, Australia (2) The Australian Mouse Brain Mapping Consortium, The University of Queensland, St Lucia, QLD, 4072, Australia Article History: Registration Date: 14/02/2013 Received Date: 22/11/2012 Accepted Date: 14/02/2013 Online Date: 10/03/2013 Article note: Electronic supplementary material The online version of this article (doi: 10.1007/s00429-013-0528-4) contains supplementary material, which is available to authorized users.
language: English
source: Cengage Learning, Inc.
identifier: ISSN: 1863-2653
fulltext: fulltext
issn:
  • 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.(Report)
creatorKharatishvili, Irina ; Shan, Zuyao Y. ; She, David T. ; Foong, Samuel ; Kurniawan, Nyoman D. ; Reutens, David C.
ispartofBrain Structure and Function, March, 2014, Vol.219(2), p.683(24)
identifierISSN: 1863-2653
subjectSeizures (Medicine) ; Magnetic Resonance Imaging ; Temporal Lobe Epilepsy
descriptionByline: Irina Kharatishvili (1), Zuyao Y. Shan (1), David T. She (1), Samuel Foong (1), Nyoman D. Kurniawan (1), David C. Reutens (1,2) Keywords: Epileptogenesis; Spontaneous recurrent seizures; Temporal lobe epilepsy; Magnetic resonance imaging; Complement; Hippocampus; Parahippocampal cortex; Epilepsy animal models Abstract: 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. Author Affiliation: (1) Centre for Advanced Imaging, The University of Queensland, St Lucia, QLD, 4072, Australia (2) The Australian Mouse Brain Mapping Consortium, The University of Queensland, St Lucia, QLD, 4072, Australia Article History: Registration Date: 14/02/2013 Received Date: 22/11/2012 Accepted Date: 14/02/2013 Online Date: 10/03/2013 Article note: Electronic supplementary material The online version of this article (doi: 10.1007/s00429-013-0528-4) contains supplementary material, which is available to authorized users.
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descriptionByline: Irina Kharatishvili (1), Zuyao Y. Shan (1), David T. She (1), Samuel Foong (1), Nyoman D. Kurniawan (1), David C. Reutens (1,2) Keywords: Epileptogenesis; Spontaneous recurrent seizures; Temporal lobe epilepsy; Magnetic resonance imaging; Complement; Hippocampus; Parahippocampal cortex; Epilepsy animal models Abstract: 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. Author Affiliation: (1) Centre for Advanced Imaging, The University of Queensland, St Lucia, QLD, 4072, Australia (2) The Australian Mouse Brain Mapping Consortium, The University of Queensland, St Lucia, QLD, 4072, Australia Article History: Registration Date: 14/02/2013 Received Date: 22/11/2012 Accepted Date: 14/02/2013 Online Date: 10/03/2013 Article note: Electronic supplementary material The online version of this article (doi: 10.1007/s00429-013-0528-4) contains supplementary material, which is available to authorized users.
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abstractByline: Irina Kharatishvili (1), Zuyao Y. Shan (1), David T. She (1), Samuel Foong (1), Nyoman D. Kurniawan (1), David C. Reutens (1,2) Keywords: Epileptogenesis; Spontaneous recurrent seizures; Temporal lobe epilepsy; Magnetic resonance imaging; Complement; Hippocampus; Parahippocampal cortex; Epilepsy animal models Abstract: 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. Author Affiliation: (1) Centre for Advanced Imaging, The University of Queensland, St Lucia, QLD, 4072, Australia (2) The Australian Mouse Brain Mapping Consortium, The University of Queensland, St Lucia, QLD, 4072, Australia Article History: Registration Date: 14/02/2013 Received Date: 22/11/2012 Accepted Date: 14/02/2013 Online Date: 10/03/2013 Article note: Electronic supplementary material The online version of this article (doi: 10.1007/s00429-013-0528-4) contains supplementary material, which is available to authorized users.
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