Long-term decrease in calbindin-D28K expression in the hippocampus of epileptic rats following pilocarpine-induced status epilepticus.

Department of Neurology, Virginia Commonwealth University School of Medicine, Richmond, VA 23298, United States.
Epilepsy Research (Impact Factor: 2.19). 06/2008; 79(2-3):213-23. DOI: 10.1016/j.eplepsyres.2008.02.006
Source: PubMed

ABSTRACT Acquired epilepsy (AE) is characterized by spontaneous recurrent seizures and long-term changes that occur in surviving neurons following an injury such as status epilepticus (SE). Long-lasting alterations in hippocampal Ca(2+) homeostasis have been observed in both in vivo and in vitro models of AE. One major regulator of Ca(2+) homeostasis is the neuronal calcium binding protein, calbindin-D28k that serves to buffer and transport Ca(2+) ions. This study evaluated the expression of hippocampal calbindin levels in the rat pilocarpine model of AE. Calbindin protein expression was reduced over 50% in the hippocampus in epileptic animals. This decrease was observed in the pyramidal layer of CA1, stratum lucidum of CA3, hilus, and stratum granulosum and stratum moleculare of the dentate gyrus when corrected for cell loss. Furthermore, calbindin levels in individual neurons were also significantly reduced. In addition, the expression of calbindin mRNA was decreased in epileptic animals. Time course studies demonstrated that decreased calbindin expression was initially present 1 month following pilocarpine-induced SE and lasted for up to 2 years after the initial episode of SE. The results indicate that calbindin is essentially permanently decreased in the hippocampus in AE. This decrease in hippocampal calbindin may be a major contributing factor underlying some of the plasticity changes that occur in epileptogenesis and contribute to the alterations in Ca(2+) homeostasis associated with AE.

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