Pharmacological Disruption of Sea Urchin Tube Foot Motility and Behavior

The understanding of the molecular basis of sea urchin behavior and sensory and motor systems lags far behind that of many other animal species. To investigate whole-animal behavior pharmacologically, we first demonstrated that immersion in drug solution is an effective drug administration route for sea urchins, whereas oral drug administration was found to be ineffective. Although intracoelomic injection was found to be effective at administering drugs, it was also found that injection itself can disrupt normal sea urchin behavior. Using the drug immersion procedure, we demonstrate that sea urchin locomotion and the sea urchin righting response are inhibited in a dose-dependent manner by the phosphodiesterase inhibitor theophylline and the transient receptor potential channel inhibitor 2-aminoethoxydiphenyl borate. The sea urchin righting response was also inhibited by the nitric oxide synthase inhibitor N(G)-nitro-l-arginine methyl ester and the Ca²⁺ channel inhibitor diltiazem, which, along with theophylline and 2-aminoethoxydiphenyl borate, would all be expected to disrupt smooth muscle function, based on studies in other animals. In addition, the removal of extracellular Ca²⁺ also inhibited the righting response, whereas an inhibitor of intracellular Ca²⁺ release, thapsigargin, did not affect the righting response, indicating that extracellular Ca²⁺ rather than intracellular Ca²⁺ stores are required for righting.