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Virginia Commonwealth University

Epileptogenesis Causes Long-Term Plasticity Changes in Calbindin D-28k in the Rat Pilocarpine Model of Acquired Epilepsy

Abstract

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.

Degree

thesis:*
Name thesis:degree_name
Master of Science
Level thesis:degree_level
Thesis
Discipline thesis:degree_discipline
Neurology
Year dc:date.available
2005

Author and committee

dc:creator, dc:contributor.*
Author dc:creator
  • Harrison, Anne Johnston
Contributors dc:contributor
  • Dr. Robert J. DeLorenzo

Subjects

dc:subject × 5

Rights

dc:rights
Statement dc:rights
  • © The Author

Identifiers

dc:identifier.*
OAI identifier oai:identifier
oai:scholarscompass.vcu.edu:etd-1854

Chain of custody

source
Harvested from
Virginia Commonwealth University
Base URL
scholarscompass.vcu.edu/do/oai/
Last updated
2026-07-24
Source record
OAI-PMH GetRecord
citation

Harrison, Anne Johnston. Epileptogenesis Causes Long-Term Plasticity Changes in Calbindin D-28k in the Rat Pilocarpine Model of Acquired Epilepsy. Thesis thesis, 2005. https://doi.org/10.25772/HTHE-FG95