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dc.contributor.authorRoche, Michael Geoffreyen_US
dc.date.accessioned2015-08-05T04:18:20Z
dc.date.available2015-08-05T04:18:20Z
dc.date.issued2012
dc.date.submitted2012
dc.identifier.other(ALMA)contemp
dc.identifier.urihttps://hdl.handle.net/2144/12604
dc.descriptionThesis (M.A.)--Boston Universityen_US
dc.description.abstractCortical spreading depression (CoSD) is a reaction of the cerebral cortex to injury and neuropathology. It is comprised of self propagating waves of neuronal hyperexcitability, followed by a pronounced and lasting depression of the electrical activity. This depression travels outward from the initiation source across the surface of the brain at a rate of 2-5 mm/min and is accompanied by a shift in the direct current potential. To better understand the mechanism behind CoSD, intra-cortical electrophysiological recording techniques were used to test the hypothesis that CoSD produces a layer-specific effect on the rat cortex. A linear multi-electrode was used to examine coherent neural activity at all levels of the primary visual cortex before, during and after CoSD. In addition, evoked neural activity was assessed by the use of paired pulse stimulation to the contralateral primary visual cortex. The effect of CoSD on the frequency content of the neural signals was also investigated. Finally, current source density analysis of the evoked signal was examined to determine whether CoSD produced alterations in the location or magnitude of where the evoked currents entered (current sinks) and left (current sources) the cortical laminae. CoSD was reliably induced, but the effects were short, only lasting for the first five minutes post initiation. Immediately following the initiation of CoSD, the first peak of the evoked potential was reduced, indicating that the excitability of the cortex was reduced by CoSD. After a period of time passed, the first peak returned to baseline while the second peak increased. The paired pulse index (ratio of the amplitude of the first evoked signal to the amplitude of the second evoked signal) was highly reduced and showed a lasting effect, indicating a reduction in the evoked inhibitory tone. This reduction in inhibitory tone was accompanied by alterations in the evoked gamma and beta bands, and a reduction in the alpha, which likely contributed in part to the reduction of the first peak. The spontaneous measured frequency bands showed a selective decrease in alpha, beta and theta, whereas gamma and delta were unaffected. All these were not specific to individual cortical lamina, but occurred at every laminae. Finally, current source density analysis showed that the CoSD did not induce any immediate or lasting changes in the pattern or magnitude of the current sinks and sources. These findings show that CoSD induces highly specific changes in the cortex, but does so in a uniform manner throughout the cortical width. The paired pulse data in conjunction with the results of the frequency analysis also suggests that CoSD causes a decrease in the efficacy of the cortical inhibitory networks. Frequency analysis further suggests that CoSD is possibly associated with a functional disconnection between the cortex and the thalamus. These data are the first to show the effects of CoSD using intracortical recordings and further the understanding of CoSD.en_US
dc.language.isoen_US
dc.publisherBoston Universityen_US
dc.rightsThis work is being made available in OpenBU by permission of its author, and is available for research purposes only. All rights are reserved to the author.en_US
dc.titleElectrophysiology of cortical spreading depression in the rat neocortexen_US
dc.typeThesis/Dissertationen_US
etd.degree.nameMaster of Artsen_US
etd.degree.levelmastersen_US
etd.degree.disciplineMedical Sciencesen_US
etd.degree.grantorBoston Universityen_US


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