The role of pannexin1 channels in seizure activity in vivo and in vitro
dc.contributor.advisor | Teskey, G. Campbell | |
dc.contributor.advisor | Thompson, Roger John | |
dc.contributor.author | Robinson, Jordan | |
dc.date.accessioned | 2017-12-18T22:34:08Z | |
dc.date.available | 2017-12-18T22:34:08Z | |
dc.date.issued | 2012 | |
dc.description | Bibliography: p. 77-85 | en |
dc.description | Some pages are in colour. | en |
dc.description.abstract | Pannexinl (Panx 1) is a large-pore channel present in the post-synaptic site that has been implicated in an in vitro model of seizure-like burst firing. However, the precise contribution of Panxl to seizure activity remains controversial, with many inconsistent findings. Furthermore, the contribution of Panxl to the development of ictogenic nervous tissue ('epileptogenesis') has not been investigated. The present experiments pursue three lines of research in an attempt to further characterize the role of Panxl in seizure and epileptogenesis. The contributions of Panxl to susceptibility to seizure, seizure severity and seizure duration were studied in vivo using both the pilocarpine model of seizure and status epilepticus, and the electrical kindling model of seizure and epileptogenesis. Further, the effect of Panx 1 block on the process of epileptogenesis itself in the electrical kindling model was examined. Finally, the role of Panxl in local excitability and short-term potentiation following epileptogenesis were studied using acute hippocampal slices obtained from kindled and sham kindled rats. A single early central infusion of Panxl blocker was sufficient to chronically attenuate epileptogenesis. Furthermore, Panxl block acutely decreased seizure severity and afterdischarge threshold in fully kindled animals in the electrical kindling model. Panxl block was also found to acutely decrease seizure severity and increase seizure latency, but not seizure duration in the pilocarpine model. Finally, Panxl block was also found to increase paired-pulse facilitation but not differentially between kindled and non-kindled tissue. | |
dc.format.extent | 85 leaves : ill. ; 30 cm. | en |
dc.identifier.citation | Robinson, J. (2012). The role of pannexin1 channels in seizure activity in vivo and in vitro (Master's thesis, University of Calgary, Calgary, Canada). Retrieved from https://prism.ucalgary.ca. doi:10.11575/PRISM/4889 | en_US |
dc.identifier.doi | http://dx.doi.org/10.11575/PRISM/4889 | |
dc.identifier.uri | http://hdl.handle.net/1880/105890 | |
dc.language.iso | eng | |
dc.publisher.institution | University of Calgary | en |
dc.publisher.place | Calgary | en |
dc.rights | University of Calgary graduate students retain copyright ownership and moral rights for their thesis. You may use this material in any way that is permitted by the Copyright Act or through licensing that has been assigned to the document. For uses that are not allowable under copyright legislation or licensing, you are required to seek permission. | |
dc.title | The role of pannexin1 channels in seizure activity in vivo and in vitro | |
dc.type | master thesis | |
thesis.degree.discipline | Neuroscience | |
thesis.degree.grantor | University of Calgary | |
thesis.degree.name | Master of Science (MSc) | |
ucalgary.item.requestcopy | true | |
ucalgary.thesis.accession | Theses Collection 58.002:Box 2117 627942987 | |
ucalgary.thesis.notes | UARC | en |
ucalgary.thesis.uarcrelease | y | en |
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