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Assessment of Memory Function in Pilocarpine-induced Epileptic Mice
Published on: June 4, 2020
Long-term decrease in calbindin-D28K expression in the hippocampus of epileptic rats following pilocarpine-induced
Dawn S Carter1, Anne J Harrison, Katherine W Falenski
1Department of Neurology, Virginia Commonwealth University School of Medicine, Richmond, VA 23298, United States.
Epilepsy Research
|April 9, 2008
Summary
Acquired epilepsy (AE) involves persistent decreases in hippocampal calbindin-D28k, a key calcium regulator. This reduction, observed after status epilepticus (SE), may contribute to epilepsy-related brain changes and calcium imbalance.
Area of Science:
- Neuroscience
- Epilepsy Research
- Calcium Homeostasis
Background:
- Acquired epilepsy (AE) involves neuronal changes after injuries like status epilepticus (SE).
- Hippocampal calcium (Ca2+) homeostasis is altered in AE models.
- Calbindin-D28k is crucial for buffering and transporting Ca2+ in neurons.
Purpose of the Study:
- To investigate hippocampal calbindin-D28k expression in a rat model of acquired epilepsy.
- To determine if calbindin levels change following pilocarpine-induced status epilepticus.
- To assess the long-term effects of SE on calbindin expression in the hippocampus.
Main Methods:
- Utilized the rat pilocarpine model to induce status epilepticus (SE).
- Quantified calbindin protein and mRNA expression in the hippocampus of epileptic and control rats.
- Corrected calbindin levels for neuronal cell loss in specific hippocampal subregions.
Main Results:
- Calbindin protein expression was significantly reduced (>50%) in the hippocampus of epileptic rats.
- Decreased calbindin was observed in CA1, CA3, hilus, and dentate gyrus, even after accounting for cell loss.
- Both calbindin protein and mRNA levels were diminished, persisting for up to two years post-SE.
Conclusions:
- Calbindin-D28k expression is persistently decreased in the hippocampus in acquired epilepsy.
- Reduced calbindin may underlie hippocampal plasticity changes and altered Ca2+ homeostasis in epileptogenesis.
- This long-lasting calbindin deficit is a significant finding in AE pathophysiology.
