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The brain-specific Beta4 subunit downregulates BK channel cell surface expression.

PloS one | Mar 22, 2012

The large-conductance K(+) channel (BK channel) can control neural excitability, and enhanced channel currents facilitate high firing rates in cortical neurons. The brain-specific auxiliary subunit β4 alters channel Ca(++)- and voltage-sensitivity, and β4 knock-out animals exhibit spontaneous seizures. Here we investigate β4's effect on BK channel trafficking to the plasma membrane. Using a novel genetic tag to track the cellular location of the pore-forming BKα subunit in living cells, we find that β4 expression profoundly reduces surface localization of BK channels via a C-terminal ER retention sequence. In hippocampal CA3 neurons from C57BL/6 mice with endogenously high β4 expression, whole-cell BK channel currents display none of the characteristic properties of BKα+β4 channels observed in heterologous cells. Finally, β4 knock-out animals exhibit a 2.5-fold increase in whole-cell BK channel current, indicating that β4 also regulates current magnitude in vivo. Thus, we propose that a major function of the brain-specific β4 subunit in CA3 neurons is control of surface trafficking.

Pubmed ID: 22438928 RIS Download

Mesh terms: Animals | Brain | CA3 Region, Hippocampal | Calcium Signaling | Cell Membrane | Down-Regulation | Electrophysiological Phenomena | Endoplasmic Reticulum | Female | HEK293 Cells | Humans | Large-Conductance Calcium-Activated Potassium Channels | Male | Mice | Mice, Inbred C57BL | Mice, Knockout | Models, Neurological | Protein Subunits | Recombinant Proteins

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Associated grants

  • Agency: NCRR NIH HHS, Id: U54 RR022241
  • Agency: NINDS NIH HHS, Id: NS052574

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