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 de¢cit in gene expression of Kcnma1 coding for the large-conductance calciumactivated potassium (BK,MaxiK) channel a-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 signi¢cant reduction in Kcnma1expression inmicrodissected dentate gyrus at different intervals after status epilepticus (24 h,10 days,1month, andmore 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 ofmesial temporal lobe epilepsy. NeuroReport19:1291-1294 © 2008 Wolters Kluwer Health LippincottWilliams & Wilkins.