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Neuroreport. 2008 Aug 27;19(13):1291-4. doi: 10.1097/WNR.0b013e3283094bb6.

Deficit of Kcnma1 mRNA expression in the dentate gyrus of epileptic rats.

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Department of Biological Sciences, The University of Texas, Brownsville/Texas Southmost College, Brownsville, Texas, USA.


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.

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