Abstract
Epileptogenesis in mesial temporal lobe epilepsy is determined by several factors including abnormalities in the expression and function of ion channels. Here, we report a long-lasting deficit in gene expression of Kcnma1 coding for the large-conductance calcium-activated potassium (BK, MaxiK) channel alpha-subunits after pilocarpine-induced status epilepticus. By using comparative real-time PCR, Taqman gene expression assays, and the delta-delta comparative threshold method we detected a significant reduction in Kcnma1 expression in microdissected dentate gyrus at different intervals after status epilepticus (24 h, 10 days, 1 month, and more than 2 months). BK channels are key regulators of neuronal excitability and transmitter release. Hence, defective Kcnma1 expression may play a critical role in the pathogenesis of mesial temporal lobe epilepsy.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Analysis of Variance
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Animals
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Dentate Gyrus / metabolism*
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Disease Models, Animal
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Down-Regulation / drug effects
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Epilepsy, Temporal Lobe / genetics*
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Gene Expression / drug effects
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Gene Expression Profiling*
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Injections, Intraperitoneal
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Injections, Subcutaneous
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Large-Conductance Calcium-Activated Potassium Channel alpha Subunits / genetics*
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Muscarinic Agonists / administration & dosage
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Muscarinic Agonists / toxicity
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Pilocarpine / administration & dosage
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Pilocarpine / toxicity
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RNA, Messenger / genetics
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RNA, Messenger / metabolism
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Rats
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Reverse Transcriptase Polymerase Chain Reaction
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Seizures / chemically induced
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Seizures / genetics
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Status Epilepticus / chemically induced
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Status Epilepticus / genetics
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Time Factors
Substances
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Kcnma1 protein, rat
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Large-Conductance Calcium-Activated Potassium Channel alpha Subunits
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Muscarinic Agonists
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RNA, Messenger
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Pilocarpine