Cyclic AMP-gated sodium current in neurons of the pedal ganglion of
Pleurobranchaea californica is activated by serotonin.
Sudlow, Leland C., and Rhanor Gillette.
Dept. of Physiology and Biophysics and the Neuroscience Program, Univ. of
Illinois, Urbana-Champaign, Urbana Ill. 61801.
APStracts 2:0031N, 1995.
SUMMARY AND CONCLUSIONS
1) We studied the roles of cAMP and cAMP-gated Na + current (I Na,cAMP ) in
the 5-HT-induced excitation of putatively serotonergic "G" neurons of
the pedal ganglion of Pleurobranchaea californica . Currents were recorded
under voltage clamp during 5-HT application and iontophoretic intracellular
cAMP injections. I Na,cAMP responses to pulsed injections of cAMP were
occluded by 5-HT-induced inward current (I 5-HT ). Occlusion was qualitatively
and quantitatively similar to that observed during steady-state activation of
I Na,cAMP by tonic iontophoretic injection of cAMP. 2) Those neurons
exhibiting occlusion of I Na,cAMP during 5-HT application also exhibited
depolarization-induced (Ca 2+ -dependent) inactivation of both I Na,cAMP and
I 5-HT . The magnitudes of the inactivation to depolarizing pulses of I 5-HT
or I Na,cAMP were similar. Recoveries from inactivation for I 5-HT and I
Na,cAMP followed similar exponentially decaying time courses. 3) The decay
rate of the I Na,cAMP response is affected by phosphodiesterase inhibitors
and can be taken as a sensitive measure of the rate of cAMP degradation (Huang
and Gillette 1991). As background steady-state I Na,cAMP was increased by
larger tonic cAMP injections, the decay rate of superimposed I Na,cAMP
responses to pulsed injections of cAMP was slowed as would be expected from
saturation of endogenous phosphodiesterase activity. The decay of I Na,cAMP
responses to pulsed cAMP injections superimposed on I 5-HT were similarly
slowed, suggesting that 5-HT action is mediated specifically by cAMP. 4) The
decay rate constants for I Na,cAMP responses to pulsed injections of cAMP
superimposed on I 5-HT did not differ from those of I Na,cAMP responses
superimposed on equivalent, background steady-state I Na,cAMP induced by
tonic injection of cAMP. Thus, 5-HT-induced changes in cAMP degradation rates
do not measurably contribute to 5-HT stimulation of endogenous cAMP. 5) These
data indicate that the inward current stimulated by serotonin in the G neurons
is largely carried by I Na,cAMP , which is stimulated by an increase in
endogenous cAMP levels. The increase in cAMP associated with I 5-HT is not
accompanied by measurable change in phosphodiesterase activity, and it is
likely due in entirety to an increase in the synthetic activity of adenylyl
cyclase.
Received 25 July 1994; accepted in final form 9 February 1995.
APS Manuscript Number J453-4.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 3 April 1995.