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Voltage‐gated K + channels play a role in cAMP‐stimulated neuritogenesis in mouse neuroblastoma N2A cells
Author(s) -
Leung YukMan,
Huang ChienFang,
Chao ChiaChia,
Lu DahYuu,
Kuo ChangShin,
Cheng TzuHurng,
Chang LiYun,
Chou ChunHsiao
Publication year - 2011
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.22430
Subject(s) - intracellular , neurite , tetraethylammonium , microbiology and biotechnology , neuroblastoma , biology , chemistry , potassium channel , biophysics , cell culture , biochemistry , in vitro , potassium , genetics , organic chemistry
Neuritogenesis is essential in establishing the neuronal circuitry. An important intracellular signal causing neuritogenesis is cAMP. In this report, we showed that an increase in intracellular cAMP stimulated neuritogenesis in neuroblastoma N2A cells via a PKA‐dependent pathway. Two voltage‐gated K + (Kv) channel blockers, 4‐aminopyridine (4‐AP) and tetraethylammonium (TEA), inhibited cAMP‐stimulated neuritogenesis in N2A cells in a concentration‐dependent manner that remarkably matched their ability to inhibit Kv currents in these cells. Consistently, siRNA knock down of Kv1.1, Kv1.4, and Kv2.1 expression reduced Kv currents and inhibited cAMP‐stimulated neuritogenesis. Kv1.1, Kv1.4, and Kv2.1 channels were expressed in the cell bodies and neurites as shown by immunohistochemistry. Microfluorimetric imaging of intracellular [K + ] demonstrated that [K + ] in neurites was lower than that in the cell body. We also showed that cAMP‐stimulated neuritogenesis may not involve voltage‐gated Ca 2+ or Na + channels. Taken together, the results suggest a role of Kv channels and enhanced K + efflux in cAMP/PKA‐stimulated neuritogenesis in N2A cells. J. Cell. Physiol. 226: 1090–1098, 2011. © 2010 Wiley‐Liss, Inc.