Increased large conductance calcium-activated potassium (BK) channel expression accompanied by STREX variant downregulation in the developing mouse CNS |
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| Authors: | Stephen H-F MacDonald Peter Ruth Hans-Guenther Knaus Michael J Shipston |
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| Affiliation: | (1) Centre for Integrative Physiology, School of Biomedical Science, Hugh Robson Building, University of Edinburgh, EH8 9XD Edinburgh, Scotland, UK;(2) Pharmacology and Toxicology, Institute of Pharmacy, University Tuebingen, 72076 Tuebingen, Germany;(3) Division for Molecular and Cellular Pharmacology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Medical University Innsbruck, Peter-Mayr Strasse 1, 6020 Innsbruck, Austria;(4) Trinity Institute of Molecular Medicine, St. James's Hospital, Dublin 8, Republic of Ireland |
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| Abstract: | Background Large conductance calcium- and voltage activated potassium (BK) channels are important determinants of neuronal excitability through effects on action potential duration, frequency and synaptic efficacy. The pore- forming subunits are encoded by a single gene, KCNMA1, which undergoes extensive alternative pre mRNA splicing. Different splice variants can confer distinct properties on BK channels. For example, insertion of the 58 amino acid stress-regulated exon (STREX) insert, that is conserved throughout vertebrate evolution, encodes channels with distinct calcium sensitivity and regulation by diverse signalling pathways compared to the insertless (ZERO) variant. Thus, expression of distinct splice variants may allow cells to differentially shape their electrical properties during development. However, whether differential splicing of BK channel variants occurs during development of the mammalian CNS has not been examined. |
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