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From the Department of Anesthesiology, Gunma University Graduate School of Medicine, Maebashi, Japan
Address correspondence and reprint requests to Shigeru Saito, Department of Anesthesiology, Gunma University Graduate School of Medicine, 33922, Showa-machi, Maebashi, 3718511 Japan. Address email to shigerus{at}showa.gunma-u.ac.jp
Neurotoxicity of local anesthetics has been reported for both matured and growing neurons. In the present study, we examined if tetracaine increases Ca2+ concentration during growth cone collapse. Intracellular Ca2+ concentration was measured by fura 2/AM after exposure to tetracaine. Tetracaine (12 mM) induced increases in intra-growth cone Ca2+ concentration (P < 0.01). The Ca2+ hot spot was expanded into the neurite from the periphery towards the cell body. When tetracaine was applied to growth cones in Ca2+ free media, the increase was minor. However, tetracaine induced growth cone collapse even in the culture media, which did not contain Ca2+. Ni2+ (100 µM; a general Ca2+ channel inhibitor) and BAPTA-AM (5 µM; intracellular Ca2+ chelator) could not inhibit growth cone collapse induced by 12 mM tetracaine. Tetracaine (>1 mM) induces collapse and Ca2+ increase at growth cones simultaneously; however, these two phenomena might be provoked independently.
IMPLICATIONS: Tetracaine induced intracellular Ca2+ increases and growth cone collapse in dorsal root ganglion neurons. The Ca2+ hot spot in the growth cone expanded into the neurite from periphery towards the cell body.
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K. Sekimoto, S. Saito, and F. Goto Tetracaine at a small concentration delayed nerve growth without destroying neurites and growth cones. Anesth. Analg., September 1, 2006; 103(3): 608 - 614. [Abstract] [Full Text] [PDF] |
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