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Induction of deflagellation by various local anesthetics in Chlamydomonas reinhardtii Dangeard (Chlamydomonadales, Chlorophyceae)
Author(s) -
Nishikawa Atsushi,
Sakamoto Yoshihiko,
Sakatoku Akihiro,
Noguchi Munenori,
Tanaka Daisuke,
Nakamura Shogo
Publication year - 2010
Publication title -
phycological research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.438
H-Index - 44
eISSN - 1440-1835
pISSN - 1322-0829
DOI - 10.1111/j.1440-1835.2010.00565.x
Subject(s) - tetracaine , dibucaine , procaine , biology , chlamydomonas , chlamydomonas reinhardtii , lidocaine , local anesthetic , biophysics , pharmacology , biochemistry , neuroscience , gene , mutant
SUMMARY Dibucaine, a local anesthetic, is known to induce flagellar excision in Chlamydomonas reinhardtii . Herein, we investigate whether other local anesthetics have similar effects. Tetracaine, bupivacaine, procaine, and lidocaine also caused flagellar excision, although their potencies were lower than that of dibucaine. Bupivacaine, procaine, and lidocaine induced a morphological change in flagella from a rod‐like shape to a disk‐like shape before flagellar excision. Except for lidocaine, these local anesthetics caused cell‐wall shedding in addition to flagellar excision. The anesthetics in order of their median effective concentration (1‐h EC 50 ) for flagellar excision are as follows: dibucaine (1.37 × 10 −5 M) < tetracaine (3.16 × 10 −5 M) < bupivacaine (4.25 × 10 −4 M) < procaine (2.02 × 10 −3 M) < lidocaine (3.61 × 10 −3 M). In all cases, Ca 2+ depletion from the solution inhibited flagellar excision. However, Ca 2+ ‐channel blockers, IP3 receptor antagonists, and inhibitors of phospholipase C did not prevent excision. We suggest that the local anesthetics induce flagellar excision by increasing the fluidity of the flagellar/cell membrane, thereby allowing extracellular Ca 2+ to flow into the cell and cause flagellar excision.