Format

Send to

Choose Destination
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.

Author information

1
Department of Biological Sciences, The University of Texas, Brownsville/Texas Southmost College, Brownsville, Texas, USA.

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.

PMID:
18695509
PMCID:
PMC2596301
DOI:
10.1097/WNR.0b013e3283094bb6
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Wolters Kluwer Icon for PubMed Central
Loading ...
Support Center