Formation of cellular projections in neural progenitor cells depends on SK3 channel activity

• DOI: 10.1111/j.1471-4159.2006.04437.x
• Publication Date: 2007-02-13T19:30:50Z
• Authors: Stefan Liebau; Bianca Vaida; Christian Proepper; Stephan Grissmer; Alexander Storch; Tobias M. Boeckers; Paul Dietl; Oliver H. Wittekindt
• Keywords: Neurons; 0301 basic medicine; Patch-Clamp Techniques; Reverse Transcriptase Polymerase Chain Reaction; Embryo, Mammalian; Immunohistochemistry; Membrane Potentials; Rats; Rats, Sprague-Dawley; Calcium Channel Agonists; Potassium Channels, Calcium-Activated; 03 medical and health sciences; Mesencephalon; Pregnancy; Animals; Benzimidazoles; Drug Interactions; Female; Pseudopodia; RNA, Messenger; Microscopy, Immunoelectron; Cells, Cultured

AbstractIon channels are potent modulators for developmental processes in progenitor cells. In a screening approach for different ion channels in neural progenitor cells (NPCs) we observed a 1‐ethyl‐2‐benzimidazolinone (1‐EBIO) activated inward current, which could be blocked by scyllatoxin (ScTX, IC50 = 2 ± 0.3 nmol/L). This initial evidence for the expression of the small conductance Ca2+ activated K+‐channel SK3 was confirmed by the detection of SK3 transcripts and protein in NPCs. Interestingly, SK3 proteins were highly expressed in non‐differentiated NPCs with a focused localization in lamellipodia as well as filopodial structures. The activation of SK3 channels using 1‐EBIO lead to an immediate filopodial sprouting and the translocation of the protein into these novel filopodial protrusions. Both effects could be prevented by the pre‐incubation of NPCs with ScTX. Our study gives first evidence that the formation and prolongation of filopodia in NPCs is, at least in part, effectively induced and regulated by SK3 channels.