Octopamine (OCT), dopamine (DA), epinephrine (EPI) and norepinephrine (NE) are endogenous excitors of the Limulus heart. The cellular sites of action of these amines were investigated by recording responses of neurones in the cardiac ganglion. There was an increase in spike frequency in pacemaker neurones, accompanied by a depolarization and an increase in the rate of repolarization of the ‘pacemaker potential’. DA also produced a transient decrease in pacemaker spike frequency which preceded its excitatory effect. All four amines produced slow, dosedependent increases in the frequency of bursting activity in cardiac ganglion follower neurones. These increases were blocked by the antagonist phentolamine. DA and NE also produced transient decreases in burst rate which were blocked by the antagonist metergoline. Local application of DA on to pacemaker cells increased follower cell burst frequency, while similar applications on to follower cells did not affect burst frequency. This indicates that DA acts directly upon pacemaker neurones to increase cardiac ganglion burst activity. In addition to their pacemaker-mediated effects, the amines also had direct effects upon follower cells. These effects were examined after eliminating follower cell bursting activity with cobalt ions. OCT and, to a smaller extent, EPI, depolarized follower cells. DA and, occasionally, NE hyperpolarized follower cells. The hyperpolarizing DA response was due to a conductance increase and was blocked by metergoline and ergonovine.

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