PIRTLE, Thomas J; SATTERLIE, Richard A; Abilene Christian University; Arizona State University: The role of cyclic GMP and cyclic AMP on mediating the modulation of Clione limacina swim behavior

The marine pteropod mollusk, Clione limacina, exhibits behaviorally relevant locomotor speed changes in response to various stimuli. Clione accelerate swimming during prey capture and as an escape response. Because Clione are negatively buoyant, they may migrate downward in the water column through inhibition of swim activity. Two neuromodulators, serotonin (5HT) and nitric oxide (NO), enhance swim acceleration in reduced preparations of Clione. In contrast, dopamine inhibits swimming in whole animals and reduced preparations of Clione. At the cellular level, 5HT enhances swim activity by changing several properties of the swim interneurons that produce the basic swim rhythm. Recently, we have begun to investigate the role of different second messenger systems in mediating changes in Clione swim speed. Bath application of the cyclic guanosine monophosphate (cGMP) analog, 8-Br-cGMP, increases swimming speed in reduced preparations. Application of 10^-3M 8-Br-cGMP changes the �sag� potential and latency to peak PIR in a way similar to 5HT. Furthermore, bath application of the guanylyl cyclase inhibitor 6-Anilinoquinoline-5,8-quinone (2.5×10^-4M) prevents serotonin-induced increases in swim acceleration. These results suggest that serotonin acts through a cGMP pathway to enhance swim speed. Application of the adenylyl cyclase activator, forskolin (10^-4M), inhibits swimming. We tested the hypothesis that dopamine acts through adenylyl cyclase to inhibit swimming by applying dopamine (10^-5M) following the application of the adenylyl cyclase inhibitor, SQ 22,536 (5.0×10^-4M). SQ 22,536 increased swim acceleration, however, addition of dopamine resulted in inhibition of swim activity. This suggests that the effects of dopamine are not mediated through a cAMP pathway.