An In Vivo Neurophysiological Model of Cortical Ischemia in the Rat

Spontaneous and evoked potentials (EPs) were recorded with cross-cortical microelectrode arrays following partial occlusion of the MCA and ACA in urethane-anaesthetised rats. The control group received no occlusion, while the treatment group was injected with anti-stroke peptide Tat-NR2B9c 5min befo...

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Bibliographic Details
Main Author: Srejic, Luka
Other Authors: Hutchison, William D.
Language:en_ca
Published: 2009
Subjects:
Rat
Online Access:http://hdl.handle.net/1807/17715
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spelling ndltd-TORONTO-oai-tspace.library.utoronto.ca-1807-177152013-11-01T04:11:24ZAn In Vivo Neurophysiological Model of Cortical Ischemia in the RatSrejic, LukaIschemiaIn vivoRatCortexTat-NR2B9cMicroelectrodesPotentials0317Spontaneous and evoked potentials (EPs) were recorded with cross-cortical microelectrode arrays following partial occlusion of the MCA and ACA in urethane-anaesthetised rats. The control group received no occlusion, while the treatment group was injected with anti-stroke peptide Tat-NR2B9c 5min before ischemia. Spontaneous EEG power significantly decreased in the stroke-only group when compared to controls (p<0.001). A greater loss of EEG power was observed on anterior electrodes closer to the occluded area versus posterior contacts in stroke-only rats (p<0.05). The Tat-NR2B9c+stroke group lost significantly less power when compared to stroke-only animals (p<0.05). EP amplitude in the stroke-only group was significantly reduced following ischemia when compared to control and Tat-NR2B9c+stroke animals (p<0.001). Epileptiform discharges were observed in 8/10 untreated stroke rats and 3/5 stroke rats treated with Tat-NR2B9c. The characteristic features of spontaneous and evoked potentials validate this rat focal stroke model for in vivo testing of pharmacological agents.Hutchison, William D.Aarts, Michelle2009-062009-09-22T21:23:07ZNO_RESTRICTION2009-09-22T21:23:07Z2009-09-22T21:23:07ZThesishttp://hdl.handle.net/1807/17715en_ca
collection NDLTD
language en_ca
sources NDLTD
topic Ischemia
In vivo
Rat
Cortex
Tat-NR2B9c
Microelectrodes
Potentials
0317
spellingShingle Ischemia
In vivo
Rat
Cortex
Tat-NR2B9c
Microelectrodes
Potentials
0317
Srejic, Luka
An In Vivo Neurophysiological Model of Cortical Ischemia in the Rat
description Spontaneous and evoked potentials (EPs) were recorded with cross-cortical microelectrode arrays following partial occlusion of the MCA and ACA in urethane-anaesthetised rats. The control group received no occlusion, while the treatment group was injected with anti-stroke peptide Tat-NR2B9c 5min before ischemia. Spontaneous EEG power significantly decreased in the stroke-only group when compared to controls (p<0.001). A greater loss of EEG power was observed on anterior electrodes closer to the occluded area versus posterior contacts in stroke-only rats (p<0.05). The Tat-NR2B9c+stroke group lost significantly less power when compared to stroke-only animals (p<0.05). EP amplitude in the stroke-only group was significantly reduced following ischemia when compared to control and Tat-NR2B9c+stroke animals (p<0.001). Epileptiform discharges were observed in 8/10 untreated stroke rats and 3/5 stroke rats treated with Tat-NR2B9c. The characteristic features of spontaneous and evoked potentials validate this rat focal stroke model for in vivo testing of pharmacological agents.
author2 Hutchison, William D.
author_facet Hutchison, William D.
Srejic, Luka
author Srejic, Luka
author_sort Srejic, Luka
title An In Vivo Neurophysiological Model of Cortical Ischemia in the Rat
title_short An In Vivo Neurophysiological Model of Cortical Ischemia in the Rat
title_full An In Vivo Neurophysiological Model of Cortical Ischemia in the Rat
title_fullStr An In Vivo Neurophysiological Model of Cortical Ischemia in the Rat
title_full_unstemmed An In Vivo Neurophysiological Model of Cortical Ischemia in the Rat
title_sort in vivo neurophysiological model of cortical ischemia in the rat
publishDate 2009
url http://hdl.handle.net/1807/17715
work_keys_str_mv AT srejicluka aninvivoneurophysiologicalmodelofcorticalischemiaintherat
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