Title
Upregulation of STREX splice variant of the large conductance Ca <sup>2+</sup>-activated potassium (BK) channel in a rat model of mesial temporal lobe epilepsy
Date Issued
01 January 2011
Access level
open access
Resource Type
journal article
Author(s)
Ermolinsky B.S.
Skinner F.
Garcia I.
Arshadmansab M.F.
Otalora L.F.P.
Zarei M.M.
Garrido-Sanabria E.R.
Abstract
Functional properties of large conductance Ca 2+ activated potassium (BK) channels are determined by complex alternative splicing of the Kcnma1 gene encoding the alpha pore-forming subunit. Inclusion of the STREX exon in a C-terminal splice site is dynamically regulated and confers enhanced Ca 2+ sensitivity and channel inhibition via cAMP-dependent phosphorylation. Here, we describe a real time quantitative PCR (qPCR) approach to investigate relative changes in the expression of STREX and ZERO splice variants using a newly designed set of probes and primers for TaqMan-based qPCR analysis of cDNA from the rat dentate gyrus at different time points following pilocarpine-induced status epilepticus. Reduction in Kcnma1 gene expression is associated with a relative increase of STREX splice variant. Relative expression of STREX variant mRNA was increased at 10 days and at more than 1 month following status epilepticus. The biological consequences of seizure-related changes in alternative splicing of Kcnma1 deserve additional investigation. © 2010 Elsevier Ireland Ltd and the Japan Neuroscience Society.
Start page
73
End page
80
Volume
69
Issue
1
Language
English
OCDE Knowledge area
Medicina básica
Neurociencias
Scopus EID
2-s2.0-78649834515
PubMed ID
Source
Neuroscience Research
ISSN of the container
01680102
Sponsor(s)
This work was supported by grants to E.R.G.S. from National Institute of Health as follows: NS063950-03 , P20MD001091 , P20MD000161 , 5SC1NS063950-04 , MBRS-RISE grant # 1R25GM06592501A1 and ARRA grant 3SC1NS063950-03S1 . F.S and M.F.A were supported by the UT System LSAMP Phase IV project founded by the National Science Foundation grant number HRD-0703584.
Sources of information:
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