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Updated: Aug 12, 2026
Isolation and Analysis of Brain-sequestered Leukocytes from Plasmodium berghei ANKA-infected Mice
Published on: January 2, 2013
Complement C5-deficient mice are protected from seizures in experimental cerebral malaria
Susan C Buckingham1, Theresa N Ramos, Scott R Barnum
1Department of Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama, U.S.A.
Abstract:
Studies have demonstrated that the membrane attack complex (MAC) of complement can evoke seizures when injected directly into rodent brain. In the course of studies that examine the role of complement in the development of experimental cerebral malaria (ECM), we observed fewer seizures in mice deficient in C5, a component required for MAC formation. To determine if the MAC contributed to the tonic-clonic seizures characteristic of ECM, we performed long-term video-electroencephalography (EEG) on C5(-/-) mice with Plasmodium berghei ANKA-induced cerebral malaria and observed significantly reduced spike and seizure frequency compared to wild-type mice. Our data suggest a role for the MAC in malaria-induced seizures and that inhibition of the terminal complement pathway may reduce seizures and seizure-related neurocognitive deficits.
Insights
The membrane attack complex (MAC) causes seizures. Inhibiting MAC formation in cerebral malaria models significantly reduced seizure activity, suggesting a therapeutic target.
Area of Science:
- Neuroscience
- Immunology
- Infectious Diseases
Background:
- The membrane attack complex (MAC) is known to induce seizures when directly applied to the brain.
- Experimental cerebral malaria (ECM) is associated with neurological complications, including seizures.
Purpose of the Study:
- To investigate the role of the MAC in seizures occurring during experimental cerebral malaria (ECM).
- To determine if inhibiting the terminal complement pathway affects seizure frequency in ECM.
Main Methods:
- Long-term video-electroencephalography (EEG) was used to monitor seizure activity.
- Comparison of seizure frequency between C5-deficient mice (lacking MAC formation) and wild-type mice infected with Plasmodium berghei ANKA.
Main Results:
- C5-deficient mice exhibited significantly reduced spike and seizure frequency compared to wild-type mice during ECM.
- This indicates a correlation between MAC formation and seizure activity in ECM.
Conclusions:
- The MAC plays a role in mediating seizures associated with malaria.
- Inhibiting the terminal complement pathway may be a viable strategy to reduce seizures and associated neurocognitive deficits in ECM.
