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Updated: Aug 14, 2026
The Pilocarpine Model of Temporal Lobe Epilepsy and EEG Monitoring Using Radiotelemetry System in Mice
Published on: February 27, 2018
Investigation of mitochondrial involvement in the experimental model of epilepsy induced by pilocarpine
Ibrahim Elias Nasseh1, Débora Amado, Esper A Cavalheiro
1Division of Neurology, Department of Neurology and Neurosurgery, Universidade Federal de São Paulo, Rua Pedro de Toledo, 781, 7 andar frente, São Paulo 04039-032, Brazil.
Abstract:
Mitochondrial abnormalities have been associated with several aspects of epileptogenesis, such as energy generation, control of cell death, neurotransmitter synthesis, and free radical (FR) production. Increased production of FRs may cause mtDNA damage leading to decreased activities of oxidative phosphorylation complexes containing mtDNA-encoded subunits. In this study, we investigated whether increased generation of FR during status epilepticus would be sufficient to provoke abnormalities in mtDNA and in the expression and activity of cytochrome c oxidase (CCO), complex IV of the respiratory chain, in the chronic phase of the pilocarpine model of temporal lobe epilepsy. DNA analysis revealed low amounts of a 4.8 kb mtDNA deletion but with no differences in frequency or quantity in the control and experimental groups. We did not find abnormalities in the expression and distribution of an mtDNA-encoded subunit of CCO (CCO-I) or a relative decrease in CCO-I when compared with nuclear-encoded subunits (CCO-IV and SDH-fp). No abnormality in CCO activity was observed through histochemistry. Although evidences of mitochondrial abnormalities were found in previously published studies, our results do not suggest that the FRs, generated during the acute phase, determined important abnormalities in mtDNA, in expression of CCO-I, and in CCO activity.
Insights
Free radicals generated during seizures do not appear to cause significant mitochondrial DNA damage or affect cytochrome c oxidase activity in the chronic phase of epilepsy. Further research is needed to understand long-term mitochondrial changes.
Area of Science:
- Neuroscience
- Mitochondrial Biology
- Epilepsy Research
Background:
- Mitochondrial dysfunction is linked to epileptogenesis, including energy deficits and cell death.
- Free radicals (FRs) may damage mitochondrial DNA (mtDNA), impacting oxidative phosphorylation.
- Cytochrome c oxidase (CCO) is a key respiratory chain complex encoded by mtDNA.
Purpose of the Study:
- To investigate if FRs during status epilepticus cause chronic mtDNA abnormalities.
- To assess the impact on CCO expression and activity in a temporal lobe epilepsy model.
Main Methods:
- Utilized the pilocarpine model of temporal lobe epilepsy.
- Performed DNA analysis for mtDNA deletions.
- Examined CCO subunit expression (CCO-I, CCO-IV, SDH-fp) via Western blotting or similar techniques.
- Assessed CCO activity using histochemistry.
Main Results:
- Identified a low amount of a 4.8 kb mtDNA deletion, with no significant difference between control and epileptic groups.
- Found no abnormalities in the expression or distribution of the mtDNA-encoded CCO-I subunit.
- Observed no relative decrease in CCO-I compared to nuclear-encoded subunits.
- Histochemical analysis showed no abnormality in CCO activity.
Conclusions:
- FRs generated during acute seizures did not lead to significant chronic mtDNA abnormalities.
- The expression and activity of CCO, a key mitochondrial enzyme, were not substantially affected in the chronic phase.
- These findings suggest that FRs during status epilepticus may not be the primary driver of chronic mitochondrial defects in this epilepsy model.
