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First published online November 14, 2008
Journal of Experimental Biology 211, 3703-3711 (2008)
Published by The Company of Biologists 2008
doi: 10.1242/jeb.023606

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Episodic swimming behavior in the nematode C. elegans

Rajarshi Ghosh^* and Scott W. Emmons

Department of Molecular Genetics, Albert Einstein College of Medicine, Bronx, NY 10461, USA

View larger version (63K): [in this window] [in a new window]   Fig. 1. In a liquid environment, after a long initial swim, worms alternate between swimming (A) and quiescence (B). (C) Typical swimming–quiescent pattern for an individual worm. 1, swimming; 0.5, slow swimming; and 0, quiescence (see Materials and methods). At time 0 the worm was transferred from the surface of solid media into liquid. (D) Swimming (gray) and quiescent (black) behavior for typical worms of five species and four C. elegans strains. N2 (Bristol) is the wild-type strain used in this study; the N2 data are from C. (E) Coiled posture in liquid (25°C) of a worm lacking ACh [cha-1(y226ts)]. (F) Sinusoidal quiescent posture of egl-4(ks60) mutant worms.

View larger version (63K): [in this window] [in a new window]   Fig. 2. (A) Effects of mutants and drug treatment on the duration of swimming (left) and quiescent (right) bouts. Data were collected starting with the first quiescent bout after the long initial swim, when the worm has entered the episodic phase of swimming. Panels 2–6: decreased GABA [unc-25(sa94ts)] and increased ACh [aldicarb, ace-1(g72);ace-2(p1000), dgk-1(nu62)] decrease swimming and increase quiescence. Panel 7: Mutation in egl-4 decreases the duration of both swimming and quiescent bouts. (B) Fraction of worms in quiescence. Left panel: in the presence of the acetylcholine esterase inhibitor aldicarb, quiescent bouts become progressively longer with time, resulting in an increasing fraction of worms in quiescence. Green, no drug; blue, 0.001 mol l–1 aldicarb; black, 0.01 mol l–1 aldicarb; yellow, 0.1 mol l–1 aldicarb. Right panel: worms lacking command interneurons cycle between swimming and quiescence immediately upon transfer into liquid, have increased quiescence, and remain sensitive to aldicarb. Yellow, glr-1::ICE, buffer; red, glr-1::ICE, 0.001 mol l–1 aldicarb; wild-type controls (green, blue) same as left panel.

View larger version (46K): [in this window] [in a new window]   Fig. 3. Effects of killing or depolarizing the command interneurons. (A) Command interneurons sustain both swimming (left panels) and quiescence (right panels). (B) Depolarization of command interneurons increases quiescence. Left and right panels as in A. (C) Progressive increase in quiescence with all command interneurons except AVB depolarized [nmr-1::GLR-1(A/T)], all command interneurons including AVB depolarized, [glr-1::GLR-1(A/T)] and AVB depolarized and the remaining command interneurons killed [glr-1::GLR-1(A/T):nmr-1::ICE]. Typical single worm swimming (gray)–quiescence (black) behavior. Wild-type data are the same as in Fig. 1D (N2, Bristol).

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