CLINICAL NEUROSCIENCE AND NEUROPATHOLOGY

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

Ermolinsky, Borisa; Arshadmansab, Massoud F.a; Pacheco Otalora, Luis F.a; Zarei, Masoud M.a b; Garrido-Sanabria, Emilio R.a b

Author Information

aDepartment of Biological Sciences, The University of Texas, Brownsville/Texas Southmost College

bThe Center for Biomedical Studies, Brownsville, Texas, USA

Correspondence to Emilio R. Garrido-Sanabria, MD, PhD, Department of Biological Sciences, 80 Fort Brown, Brownsville, TX 78520, USA

Tel: +1 956 882 5053; fax: +1 956 882 5043; e-mail: [email protected]

Received 26 April 2008; accepted 18 May 2008

NeuroReport 19(13):p 1291-1294, August 27, 2008. | DOI: 10.1097/WNR.0b013e3283094bb6

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 α-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.

© 2008 Lippincott Williams & Wilkins, Inc.

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