Fictive locomotion induced by octopamine in the earthworm
Kenji Mizutani1,
Hiroto Ogawa2,
Junichi Saito3 and
Kotaro Oka1,3,4,*
1 Center for Life Science and Technology, School of Fundamental Science and Technology, Keio University, 3-14-1 Hiyoshi, Kohoku-ku, Yokohama 223-8522, Japan,
2 Department of Biology, Saitama Medical School, 981 Kawakado, Moroyama, Iruma-gun, Saitama 350-0496, Japan,
3 Institute of Biomedical Engineering, Faculty of Science and Technology, Keio University, 3-14-1 Hiyoshi, Kohoku-ku, Yokohama 223-8522, Japan and
4 Department of System Design Engineering, Faculty of Science and Technology, Keio University, 3-14-1 Hiyoshi, Kohoku-ku, Yokohama 223-8522, Japan
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Fig. 1. Circular muscle contraction induced by OA. (A) Diagram of a semi-intact preparation. In the middle part of the dissected body wall, a small hook is connected to a force transducer via a pulley. Electrical activities of motor neurons were simultaneously recorded from the cut end of the first segmental nerve in the same segment using a glass suction electrode. (B) Strong phasic contractions could be observed on application of 10–4 mol l–1 OA (upper trace). In the absence of the ventral nerve cord, no contractions were observed under the same experimental conditions (lower trace). Downward deflections of the force response indicate a circular muscle contraction. The broken lines indicate when the concentration of OA was changed. Open triangles, resting level contraction; solid triangles, strong contraction associated with crawling behavior. (C) The results of simultaneous recording of muscle contraction and electrical activity from motor neurons. In control preparations, electrical activity was only seen at the onset of a contraction. At 10–4 mol l–1 OA, electrical activity occurred throughout much of the period of contraction.
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Fig. 2. Extracellular recordings of motor outputs from the first lateral nerves. (A) Schematic diagram showing configuration of suction electrodes. Right and left first lateral nerves in the same segment were suctioned to record motor activity patterns. (B) Neural activity from the right (R) and left (L) first lateral nerves was synchronized. The distance between broken lines signifies burst duration. The solid circles indicate spikes of large amplitude. (C) Extended recording time from the first lateral nerves. The arrowheads indicate burst activity. (D) At 10–4 mol l–1, constant burst activity was observed in comparison with the control condition. The bars above each trace mark the occurrence of a crawling episode.
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Fig. 3. Burst period (BP) and its coefficient of variance as a function of concentration (N=6). (A) We measured the BP and counted the number of bursts from 2 to 5 min after OA application. (B) A significant increase in the frequency of burst activity was observed for OA concentrations in the range from 10–6 mol l–1 to 10–4 mol l–1. The coefficient of variation (the square root of BP variance divided by its mean) was small during fictive locomotion. Solid circles, burst frequency; open circles, coefficient of variance.
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Fig. 4. Motor output recorded from first lateral nerves of three (anterior, middle and posterior) segmental ganglia separated by intervening segments. (A) Experimental setup. (B) Bursts propagated along VNC. Arrowheads signify the timing of highest amplitude spikes in bursts. Bars (indicated by solid triangles) are latencies. In this case, the distances between the anterior and middle electrodes, and middle and posterior electrodes, are 0.6 and 1.8 mm, respectively. (C) Propagation velocity of bursts along VNC (N=6). The propagation velocity was approximately 60–110 mm s–1, and increased with increasing octopamine concentration. Values are means ± S.D. A noticeable increase in propagation velocity was observed for octopamine concentrations between 10–6 mol l–1 and 10–3 mol l–1.
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© The Company of Biologists Ltd 2002
