Cyclic Adenosine Monophosphate Mediation of Peptide Neurohormone Effects on the Lobster Cardiac Ganglion

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Abstract
Two cardioexcitors which can be extracted or released from crustacean neurohaemal structures, the pericardial organs, alter the endogenous bursting activity of isolated lobster cardiac ganglia in different ways. A small peptide increases the burst frequency of the ganglion, the duration of each burst, and the number of spikes per burst, while 5-hydroxytryptamine (5-HT) increases burst frequency, but decreases the burst duration and number of spikes per burst. Four lines of evidence are presented that cyclic adenosine monophosphate (cAMP) mediates the effects of peptide on the ganglion, but does not play a significant role in 5-HT action: (1) exogenous cAMP mimics the effects of peptide but not of 5-HT on burst parameters; (2) inhibition of the enzyme phosphodiesterase, which increases endogenous levels of cAMP, mimics the effects of peptide and potentiates peptide action but not that of 5-HT; (3) putative blockers of adenylate cyclase block the action of peptide but not of 5-HT; (4) peptide causes a large increase in cAMP content of the ganglion, while 5-HT application results in a much smaller increase.