Cellular Mechanisms Underlying Swim Acceleration in the Pteropod Mollusk Clione limacina1

The pteropod mollusk Clione limacina swims by dorsal-ventral flapping movements of its wing-like parapodia. Two basic swim speeds are observed—slow and fast. Serotonin enhances swimming speed by increasing the frequency of wing movements. It does this by modulating intrinsic properties of swim inter...

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Bibliographic Details
Published in:Integrative and Comparative Biology
Main Authors: Thomas J. Pirtle, Richard A. Satterlie
Format: Text
Language:English
Published: The Society for Integrative and Comparative Biology 2004
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Online Access:https://doi.org/10.1093/icb/44.1.37
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Summary:The pteropod mollusk Clione limacina swims by dorsal-ventral flapping movements of its wing-like parapodia. Two basic swim speeds are observed—slow and fast. Serotonin enhances swimming speed by increasing the frequency of wing movements. It does this by modulating intrinsic properties of swim interneurons comprising the swim central pattern generator (CPG). Here we examine some of the ionic currents that mediate changes in the intrinsic properties of swim interneurons to increase swimming speed in Clione. Serotonin influences three intrinsic properties of swim interneurons during the transition from slow to fast swimming: baseline depolarization, postinhibitory rebound (PIR), and spike narrowing. Current clamp experiments suggest that neither Ih nor IA exclusively accounts for the serotonin-induced baseline depolarization. However, Ih and IA both have a strong influence on the timing of PIR—blocking Ih increases the latency to PIR while blocking IA decreases the latency to PIR. Finally, apamin a blocker of IK(Ca) reverses serotonin-induced spike narrowing. These results suggest that serotonin may simultaneously enhance Ih and IK(Ca) and suppress IA to contribute to increases in locomotor speed.