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Synopsis   Both nitric oxide (NO) and serotonin (5HT) mediate swim acceleration in the marine mollusk,  Clione    limacina . In this study, we examine the role that the second messenger, cyclic guanosine monophosphate (cGMP), plays in mediating NO and 5HT-induced swim acceleration. We observed that the application of an analog of cGMP or an activator of soluble guanylyl cyclase (sGC) increased fictive locomotor speed recorded from Pd-7 interneurons of the animal’s locomotor central pattern generator. Moreover, inhibition of sGC decreased fictive locomotor speed. These results suggest that basal levels of cGMP are important for slow swimming and that increased production of cGMP mediates swim acceleration in  Clione . Because NO has its effect through cGMP signaling and because we show herein that cGMP produces cellular changes in  Clione  swim interneurons that are consistent with cellular changes produced by 5HT application, we hypothesize that both NO and 5HT function via a common signal transduction pathway that involves cGMP. Our results show that cGMP mediates NO-induced but not 5HT-induced swim acceleration in  Clione .

integrative organismal biology

Cyclic Guanosine Monophosphate Modulates Locomotor Acceleration Induced by Nitric Oxide but not Serotonin in<i>Clione limacina</i>Central Pattern Generator Swim Interneurons

Cyclic Guanosine Monophosphate Modulates Locomotor Acceleration Induced by Nitric Oxide but not Serotonin inClione limacinaCentral Pattern Generator Swim Interneurons