{"id":{"repo_id":"vcu","oai_identifier":"oai:scholarscompass.vcu.edu:etd-1854"},"canonical_url":"https://search.dev.ndltd.org/etd/vcu/oai:scholarscompass.vcu.edu:etd-1854","repository":{"repo_id":"vcu","name":"Virginia Commonwealth University","base_url":"https://scholarscompass.vcu.edu/do/oai/"},"display":{"title":"Epileptogenesis Causes Long-Term Plasticity Changes in Calbindin D-28k in the Rat Pilocarpine Model of Acquired Epilepsy","abstract":"Epilepsy is one of the most common neurological disorders, affecting more than 2% of children and 1% of adults in the U.S. Emerging research has demonstrated that calcium, as a major second messenger system, underlies many of these injury-induced plasticity changes associated with the development of epilepsy. Recent evidence has suggested that long term elevations in neuronal resting calcium levels play a role in initiating and maintaining epileptogenesis (the development of epilepsy). Collaborations between our lab and others have produced microarray data that suggests that a major calcium-binding protein, calbindin D-28k, mRNA levels are decreased in epileptic rats even up to one year following pilocarpine treatment. The goal of this research effort was to determine if epileptogenesis alters basal calcium levels by producing a long-term change in the expression of the major calcium binding protein in neurons, calbindin D-28k. Immunohistochemistry (MC) and western blot experiments have been conducted to test the hypothesis that epileptogenesis produces a long lasting decrease in the expression of calbindin in the hippocampus in the rat pilocarpine model of acquired epilepsy. IHC experiments indicated that changes in calbindin expression occur gradually over a 2-4 week interval after the initial injury. Significant decreases in calbindin immunoreactivity are seen in the hippocampus of epileptic animals, at one month, four months, and six months post-pilocarpine treatment. However, these changes were not seen as early as 4 days post-status epilepticus. Western blots quantitated differences between epileptic animals and naive controls. Long lasting decreases in calbindin may play an important role in the altered calcium homeostatic mechanisms observed in epileptic neurons. These findings will help to elucidate one of many changes that occurs in epilepsy.","abstract_html":"Epilepsy is one of the most common neurological disorders, affecting more than 2% of children and 1% of adults in the U.S. Emerging research has demonstrated that calcium, as a major second messenger system, underlies many of these injury-induced plasticity changes associated with the development of epilepsy. Recent evidence has suggested that long term elevations in neuronal resting calcium levels play a role in initiating and maintaining epileptogenesis (the development of epilepsy). Collaborations between our lab and others have produced microarray data that suggests that a major calcium-binding protein, calbindin D-28k, mRNA levels are decreased in epileptic rats even up to one year following pilocarpine treatment. The goal of this research effort was to determine if epileptogenesis alters basal calcium levels by producing a long-term change in the expression of the major calcium binding protein in neurons, calbindin D-28k. Immunohistochemistry (MC) and western blot experiments have been conducted to test the hypothesis that epileptogenesis produces a long lasting decrease in the expression of calbindin in the hippocampus in the rat pilocarpine model of acquired epilepsy. IHC experiments indicated that changes in calbindin expression occur gradually over a 2-4 week interval after the initial injury. Significant decreases in calbindin immunoreactivity are seen in the hippocampus of epileptic animals, at one month, four months, and six months post-pilocarpine treatment. However, these changes were not seen as early as 4 days post-status epilepticus. Western blots quantitated differences between epileptic animals and naive controls. Long lasting decreases in calbindin may play an important role in the altered calcium homeostatic mechanisms observed in epileptic neurons. These findings will help to elucidate one of many changes that occurs in epilepsy.","abstract_has_math":false,"creators":["Harrison, Anne Johnston"],"institution":null,"degree_name":"Master of Science","degree_level":"Thesis","degree_discipline":"Neurology","degree_department":null,"school":null,"contributors":["Dr. Robert J. DeLorenzo"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2005,"date_issued":"2005-01-01T08:00:00Z","date_published":"2005-01-01T08:00:00Z","updated_at":"2026-07-24T05:54:30Z","subjects":["binding protein","calcium","Medical Specialties","Medicine and Health Sciences","Neurology"],"languages":[],"rights":["© The Author"],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["https://scholarscompass.vcu.edu/etd/855"],"render_values":[{"text":"https://scholarscompass.vcu.edu/etd/855","href":"https://scholarscompass.vcu.edu/etd/855","code":true}]}]},"links":{"outbound_url":"https://doi.org/10.25772/HTHE-FG95","outbound_label":"DOI","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Dr. Robert J. 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Recent evidence has suggested that long term elevations in neuronal resting calcium levels play a role in initiating and maintaining epileptogenesis (the development of epilepsy). Collaborations between our lab and others have produced microarray data that suggests that a major calcium-binding protein, calbindin D-28k, mRNA levels are decreased in epileptic rats even up to one year following pilocarpine treatment. The goal of this research effort was to determine if epileptogenesis alters basal calcium levels by producing a long-term change in the expression of the major calcium binding protein in neurons, calbindin D-28k. Immunohistochemistry (MC) and western blot experiments have been conducted to test the hypothesis that epileptogenesis produces a long lasting decrease in the expression of calbindin in the hippocampus in the rat pilocarpine model of acquired epilepsy. IHC experiments indicated that changes in calbindin expression occur gradually over a 2-4 week interval after the initial injury. Significant decreases in calbindin immunoreactivity are seen in the hippocampus of epileptic animals, at one month, four months, and six months post-pilocarpine treatment. However, these changes were not seen as early as 4 days post-status epilepticus. Western blots quantitated differences between epileptic animals and naive controls. Long lasting decreases in calbindin may play an important role in the altered calcium homeostatic mechanisms observed in epileptic neurons. These findings will help to elucidate one of many changes that occurs in epilepsy."]},{"key":"dc:title","label":"Title","values":["Epileptogenesis Causes Long-Term Plasticity Changes in Calbindin D-28k in the Rat Pilocarpine Model of Acquired Epilepsy"]}]}],"canonical_facts":{"dc:contributor":["Dr. Robert J. DeLorenzo"],"dc:creator":["Harrison, Anne Johnston"],"dc:date.available":["2014-07-09T07:00:00Z"],"dc:description.abstract":["Epilepsy is one of the most common neurological disorders, affecting more than 2% of children and 1% of adults in the U.S. Emerging research has demonstrated that calcium, as a major second messenger system, underlies many of these injury-induced plasticity changes associated with the development of epilepsy. Recent evidence has suggested that long term elevations in neuronal resting calcium levels play a role in initiating and maintaining epileptogenesis (the development of epilepsy). Collaborations between our lab and others have produced microarray data that suggests that a major calcium-binding protein, calbindin D-28k, mRNA levels are decreased in epileptic rats even up to one year following pilocarpine treatment. The goal of this research effort was to determine if epileptogenesis alters basal calcium levels by producing a long-term change in the expression of the major calcium binding protein in neurons, calbindin D-28k. Immunohistochemistry (MC) and western blot experiments have been conducted to test the hypothesis that epileptogenesis produces a long lasting decrease in the expression of calbindin in the hippocampus in the rat pilocarpine model of acquired epilepsy. IHC experiments indicated that changes in calbindin expression occur gradually over a 2-4 week interval after the initial injury. Significant decreases in calbindin immunoreactivity are seen in the hippocampus of epileptic animals, at one month, four months, and six months post-pilocarpine treatment. However, these changes were not seen as early as 4 days post-status epilepticus. Western blots quantitated differences between epileptic animals and naive controls. Long lasting decreases in calbindin may play an important role in the altered calcium homeostatic mechanisms observed in epileptic neurons. These findings will help to elucidate one of many changes that occurs in epilepsy."],"dc:identifier":["https://doi.org/10.25772/HTHE-FG95","https://scholarscompass.vcu.edu/etd/855"],"dc:rights":["© The Author"],"dc:subject":["binding protein","calcium","Medical Specialties","Medicine and Health Sciences","Neurology"],"dc:title":["Epileptogenesis Causes Long-Term Plasticity Changes in Calbindin D-28k in the Rat Pilocarpine Model of Acquired Epilepsy"],"thesis:degree_discipline":["Neurology"],"thesis:degree_level":["Thesis"],"thesis:degree_name":["Master of Science"]},"updated_at":"2026-07-24T05:54:30Z"}