Feedback from motor neurones to pacemaker neurones in lobster cardiac ganglion contributes to regulation of burst frequency

The crustacean cardiac ganglion has traditionally been viewed as a two-layered system in which pacemaking is a function of the four small cells which trigger the five follower motor neurones via chemical and electrotonic synaptic excitation. The work reported here shows that there is strong feedback from motor neurones to small cells, by which endogenous burst-organizing potentials (driver potentials or DPs) and their hyperpolarizing afterpotentials contribute to regulation of bursting frequency. Isolated cardiac ganglia were placed in a two-chamber perfusion system which allowed independent treatment of small cells and motor neurones. When the motor neurones were silenced with tetrodotoxin (TTX), the small cells continued organizing bursts of activity which recurred at an average frequency 41% higher than bursting by normal ganglia in saline. The average burst duration was not altered. Driver potentials were evoked in TTX-treated motor neurones by electrical stimulation, by ionic alteration of the medium, or by treatment with the cardioexcitor peptide proctolin. DPs which occurred synchronously with small-cell bursts prolonged and intensified the bursts (more spikes per burst). When DPs were evoked in motor neurones during the interburst interval, they triggered small-cell bursts even at very short intervals after a spontaneous burst had occurred. All small-cell bursts which were associated with motor neurone DPs were followed by interburst intervals of longer than normal duration. The decrease in instantaneous burst frequency (increase in total burst cycle duration) caused by motor neurone DPs wai similar in magnitude to the drop in burst frequency observed when the ganglion recovered normal activity after TTX washout.