Mechanosensitivity of voltage-gated K⁺ currents in rat trigeminal ganglion neurons

다국어 초록 (Multilingual Abstract)

<P>We investigated the mechanosensitivity of voltage-gated K<SUP>+</SUP> channel (VGPC) currents by using whole-cell patch clamp recording in rat trigeminal ganglion (TG) neurons. On the basis of biophysical and pharmacological properties, two types of VGPC currents were isolated. One was transient (I<SUB>K,A</SUB>), the other sustained (I<SUB>K,V</SUB>). Hypotonic stimulation (200 mOsm) markedly increased both I<SUB>K,A</SUB> and I<SUB>K,V</SUB> without affecting their activation and inactivation kinetics. Gadolinium, a well-known blocker of mechanosensitive channels, failed to block the enhancement of I<SUB>K,A</SUB> and I<SUB>K,V</SUB> induced by hypotonic stimulation. During hypotonic stimulation, cytochalasin D, an actin-based cytoskeletal disruptor, further increased I<SUB>K,A</SUB> and I<SUB>K,V</SUB>, whereas phalloidin, an actin-based cytoskeletal stabilizer, reduced I<SUB>K,A</SUB> and I<SUB>K,V</SUB>. Confocal imaging with Texas red-phalloidin showed that actin-based cytoskeleton was disrupted by hypotonic stimulation, which was similar to the effect of cytochalasin D. Our results suggest that both I<SUB>K,A</SUB> and I<SUB>K,V</SUB> are mechanosensitive and that actin-based cytoskeleton is likely to regulate the mechanosensitivity of VGPC currents in TG neurons. © 2006 Wiley-Liss, Inc.</P>