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 α-subunits after pilocarpine-induced status epilepticus. By using comparative realtime 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.
Ermolinsky, B., Arshadmansab, M. F., Pacheco Otalora, L. F., Zarei, M. M., & Garrido-Sanabria, E. R. (2008). Deficit of Kcnma1 mRNA expression in the dentate gyrus of epileptic rats. Neuroreport, 19(13), 1291–1294. https://doi.org/10.1097/WNR.0b013e3283094bb6
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