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Targeting BK (big potassium) channels in epilepsy
1Georgetown University Medical Center, Interdisciplinary Program in Neuroscience and Department of Pediatrics, Washington, DC 20057, USA. pn@georgetown.edu
Expert Opinion on Therapeutic Targets
|September 20, 2011
Summary
Large conductance, Ca2+-activated K+ (BKCa) channels are implicated in epilepsy. Both loss-of-function and gain-of-function mutations in BKCa channels can cause seizures, suggesting they are potential drug targets.
Area of Science:
- Neuroscience
- Molecular Biology
- Epileptology
Background:
- Epilepsies are neurological disorders characterized by recurrent seizures due to neuronal hyperexcitability.
- Ion channels, crucial for neuronal excitability, are implicated in epilepsy.
- Large conductance, Ca2+-activated K+ (BKCa) channels play a significant role in seizure etiology.
Purpose of the Study:
- To review the structure-function of BKCa channels.
- To elucidate the role of BKCa channels in epilepsy pathophysiology.
Main Methods:
- Literature review on BKCa channel structure-function.
- Analysis of BKCa channel involvement in various epilepsy models and human epilepsy.
Main Results:
- Loss-of-function BKCa channel mutations are linked to temporal lobe epilepsy, tonic-clonic seizures, and alcohol withdrawal seizures.
- BKCa channel blockade can induce seizures and status epilepticus.
- Gain-of-function mutations in BKCa channel subunits can lead to idiopathic epilepsy, particularly absence epilepsy.
Conclusions:
- Both loss-of-function and gain-of-function BKCa channel alterations contribute to epilepsy.
- BKCa channels represent potential therapeutic targets for suppressing specific seizure phenotypes, including temporal lobe and absence seizures.
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