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Bcl-w protects hippocampus during experimental status epilepticus
Brona Murphy1, Mark Dunleavy, Sachiko Shinoda
1Department of Physiology and Medical Physics, Royal College of Surgeons in Ireland, 123 St. Stephen's Green, Dublin 2, Ireland.
The American Journal of Pathology
|August 19, 2007
Summary
Bcl-w protein protects against seizure-induced neuronal death in the hippocampus. Lower Bcl-w levels exacerbate neuronal loss and increase seizure activity, suggesting a neuroprotective role in temporal lobe epilepsy.
Area of Science:
- Neuroscience
- Cell Biology
- Epilepsy Research
Background:
- Seizures activate mitochondrial cell death pathways.
- Bcl-2 family proteins regulate mitochondrial dysfunction but their role in epilepsy is unclear.
- Hippocampal neurons are vulnerable to seizure-induced death.
Purpose of the Study:
- To investigate the mitochondrial cell death pathway in seizure-induced neuronal death.
- To determine the role of anti-apoptotic Bcl-2 proteins, specifically Bcl-w, in this process.
- To examine Bcl-w levels in temporal lobe epilepsy patients.
Main Methods:
- Induced status epilepticus in mice using intra-amygdala kainic acid.
- Analyzed hippocampal tissue for markers of apoptosis and Bcl-2 family protein levels.
- Compared seizure-induced neuronal injury in Bcl-w-deficient mice versus wild-type mice.
- Performed quantitative electroencephalography (qEEG) to assess seizure activity.
- Measured Bcl-w levels in human temporal lobe epilepsy patient hippocampus.
Main Results:
- Seizures induced cytochrome c release, caspase activation, and neuronal death in the hippocampus.
- Hippocampal Bcl-w levels significantly decreased after seizures, unlike Bcl-2 or Bcl-xl.
- Bcl-w-deficient mice exhibited increased hippocampal CA3 neuronal loss and DNA fragmentation post-seizure.
- Bcl-w deficiency led to earlier seizure onset and polyspike activity.
- Elevated Bcl-w levels were found in the hippocampus of temporal lobe epilepsy patients.
Conclusions:
- Bcl-w acts as an endogenous neuroprotectant against seizure-induced neuronal death.
- Loss of Bcl-w function exacerbates hippocampal injury and alters seizure neurophysiology.
- Bcl-w may possess seizure-suppressive functions relevant to temporal lobe epilepsy.
