| Abstract No.: | C-C3101 |
| Country: | Canada |
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| Title: | ATTENUATION OF EVOKED CORTICAL POTENTIALS AND LOSS OF EEG POWER IN A RAT FOCAL STROKE MODEL
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| Authors/Affiliations: | 1 Luka Srejic*; 2 Joan Forder; 3 Michelle Aarts; 1 William Hutchison;
1 Department of Physiology, Faculty of Medicine, University of Toronto, ON, Canada; 2 Division of Fundamental Neurobiology, Toronto Western Research Institute, ON, Canada; 3 Life Sciences, Biology, University of Toronto at Scarborough, ON, Canada
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| Content: | Objectives: To create a stable neurophysiological model of permanent focal ischemia that can be used for pharmacological experimentation and in vivo evaluation of antistroke therapies.
Materials and methods: Spontaneous and evoked cortical potentials were recorded with a parasagittal 8 channel tungsten microelectrode array before, during and up to 3 hours following cauterization of the distal branches of the middle cerebral artery (MCA) in 17 urethane-anaesthetized rats. A bipolar thalamic stimulating (20 – 120 uA) electrode recorded early (3 - 10ms) and late (100, 300 ms) components to single and double pulses (50ms interval). Spontaneous and evoked cortical potentials were recorded at a depth of 2mm from the cortical surface since this yielded the strongest evoked potentials in 6 rats. Cortical blood flow was measured for the duration of the experiment using an 80mm laser Doppler probe positioned near the ischemic core. Control experiments were performed in 5 rats with the same time course but without arterial coagulation. Fast fourier transforms of 8 channel EEG depth electrodes were taken and the area under curve (AUC) of the low frequency oscillations (2 – 8 Hz) at 20 min and 1 hour post stroke were analyzed after normalization with baseline. Three way ANOVA (with post hoc comparisons) was used to determine significance of EEG power loss.
Results: Fibre volleys and early synaptic components were attenuated by 1min and recovered to baseline by 3 – 4 mins, while late components returned to their pre-ischemic levels within 10 min. The amplitude of the first negative component was potentiated to almost 200% of baseline at 3 – 4 min but returned to baseline by 7 mins. This transient potentiation may reflect the post-ischemic release of glutamate implicated in excitotoxic cell death. At 20 min and 1 h post stroke spontaneous EEG activity showed similar decreases in power by 71% across all electrodes compared to sham recordings (ANOVA F= 290, d.f.=1,1, p<0.001). A greater loss of EEG power was observed on electrodes closer to the centre of the array (ANOVA F=14, d.f.=7, p<0.001). Epileptiform discharges of 5 Hz rhythmic spiking were observed in some animals 20 – 30 min post stroke. Discharges were initially 2 - 4s in duration near central electrodes then propagated outward with progressively longer durations (up to 20 – 30s). In ischemic rats cortical blood flow dropped by 22% of sham recordings baseline by 20 min (one tailed t test, p < 0.001) and 51% by 1 h (p<0.001).
Conclusion: The characteristic features of spontaneous and thalamic evoked cortical potentials validate this rat focal stroke model for in vivo testing of pharmacological agents that block excitotoxic sequelae and epileptiform discharges following acute stroke.
Supported by Canadian Stroke Network (CSN) |
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