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Cellular Mechanisms Underlying Swim Acceleration in the Pteropod Mollusk Clione limacina
Author(s) -
Thomas J. Pirtle
Publication year - 2004
Publication title -
integrative and comparative biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.328
H-Index - 123
eISSN - 1557-7023
pISSN - 1540-7063
DOI - 10.1093/icb/44.1.37
Subject(s) - depolarization , neuroscience , serotonin , interneuron , electrophysiology , biology , biophysics , anatomy , inhibitory postsynaptic potential , chemistry , biochemistry , receptor
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 I(h) nor I(A) exclusively accounts for the serotonin-induced baseline depolarization. However, I(h) and I(A) both have a strong influence on the timing of PIR-blocking I(h) increases the latency to PIR while blocking I(A) decreases the latency to PIR. Finally, apamin a blocker of I(K(Ca)) reverses serotonin-induced spike narrowing. These results suggest that serotonin may simultaneously enhance I(h) and I(K(Ca)) and suppress I(A) to contribute to increases in locomotor speed.

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