Spontaneous electrical activity and interaction of large and small cells in cardiac ganglion of the crab, Portunus sanguinolentus

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Abstract
Semi-isolated preparations of the 9-celled cardiac ganglion of the crab P. sanguinolentus were studied electrophysiologically, using simultaneous recording from extracellular and 2 or 3 intracellular electrodes. Three large (80 .times. 120 .mu.m) cells lie near the anterior end of the 5 mm main trunk; 2 large and 4 small (< 50 .mu.m) cells at the posterior end. Large-cell axons pass along the main trunk and exit to innervate cardiac muscle; small-cell axons do not leave the ganglion. The semi-isolated ganglion produces spontaneous electrical activity organized into regularly patterned, rhythmic bursts of large- and small-cell impulses recurring at rates of 0.3-0.6/s and lasting 500-800 ms. Intracellular recordings from small cells show a slow pacemaker depolarization from a maximum membrane potential of -54 mV leading with only a slight inflection at approximately -50 mV to a depolarized plateau at approximately -40 mV. Depolarizations from large cells represent excitatory postsynaptic potentials (EPSP) corresponding with individual small-cell impulses, attenuated, non-overshooting spikes and an underlying slow depolarization; usually no pacemaker depolarization is apparent between bursts. EPSP, impulses and the slow depolarization occur synchronously among the large cells. Intracellular recordings from large-cell axons 4 mm from the soma show overshooting action potentials arising sharply from a base line. Current passing with electrodes intracellular to 2 cells has established directly that all large cells are electrotonnically coupled and that an anterior cell and a small cell are coupled. Current-voltage relations and coupling coefficients measured in ganglia are made quiescent by perfusion with 3 .times. 10-7 M tetrodotoxin (TTX). Intracellular recording from small cells showed that the effectiveness of current passed into large cells in altering spontaneous burst rhythm depends on electrotonic alteration of the small-cell potential. Small cells act as pacemakers and control burst rhythm. Ganglia perfused with saline having 1/3 Ca, 3 .times. Mg show disappearance of the sustained depolarization underlying bursts, inhibition of EPSP, nonbursting, steady but synchronous firing of large-cell impulses and irregular firing of small cells. The effects of both treatments are reversible. Chemically mediated synaptic transmission is not sufficient to ensure rhythmic bursting. An essential role of the slow, underlying depolarization in generation of bursts is suggested.