Does extra-hippocampal sprouting accompany epileptogenesis?

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dc.contributor.authorWallace, Amy Elizabethen_US
dc.date.accessioned2024-08-15T20:13:43Z
dc.date.available2024-08-15T20:13:43Z
dc.date.copyright2002en_US
dc.date.issued2002
dc.degree.departmentDepartment of Psychology
dc.degree.levelMaster of Arts M.A.en
dc.description.abstractTo determine whether extra-hippocampal axonal sprouting occurs in association with epileptiform activity I used two preparations: kainic acid-induced status epilepticus and kindling. Tissue from rats was collected five and 30 days after status epilepticus and following five stimulations or five stage five seizures in amygdaloid kindled rats. Using antibodies for synaptophysin and GAP-43, as well as Timm staining, the tissue was processed and analyzed for axonal sprouting. As previously described, rats treated with kainic acid as well as rats kindled to five stage five seizures displayed an increase in Timm granules in the inner molecular layer of the dentate gyrus. Furthermore, five days following kainic acid-induced status epilepticus, there was an increase in synaptophysin immunoreactivity in the inner molecular layer of the dentate gyrus. Nevertheless, there were no changes in immunoreactivity or Timm stain observed in the piriform cortex, the perirhinal cortex or the basolateral amygdala. As suggested by these results, extra-hippocampal axonal sprouting may not occur following epileptogenesis. However, it is also plausible that the changes are subtle and remained undetected by the methods of quantification I used. Furthermore, mechanisms other than axonal sprouting may be responsible for epileptogenesis.
dc.format.extent118 pages
dc.identifier.urihttps://hdl.handle.net/1828/20070
dc.rightsAvailable to the World Wide Weben_US
dc.titleDoes extra-hippocampal sprouting accompany epileptogenesis?en_US
dc.typeThesisen_US

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