Ionic bases of slow, depolarizing responses of cardiac ganglion neurons in the crab, Portunus sanguinolentus

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Abstract
The effect of changes was examined in the ionic composition of the perfusing saline on the tetrodotoxin-resistant, regenerative, slow depolarizing responses to brief depolarizing current, termed driver potentials, shown by large neurons of the crab (P. sanguinolentus) cardiac ganglion. In semi-isolated ganglia, intracellular recordings were made from 2 or 3 cells simultaneously; current was passed via a bridge or with a second intracellular electrode. Tetrodotoxin (TTX), 3 .times. 10-7 M, was continuously perfused throughout all the experiments. The amplitude and rates of rise and fall are changed in direct proportion to the log [Ca]o [outside Ca concentration], tested over the range 2.6-26 mM (normal, 13 mM). Driver potential responses are eliminated by addition to the saline of 4 mM Mn or 0.5 mM La. Mn, but not La, inhibition is reversible. The addition of 50 mM tetraethylammonium chloride (TEA) to TTX-containing saline leads to increased input resistance of 25%, increased rate of rise, peak amplitude and duration of driver potential responses. In the presence of TEA or procaine (1-7 mM), regenerative responses of constant amplitude and form can be elicited at rates as high as 1/s, as compared with rates of < 0.15/s in their absence. In the presence of TTX + TEA or procaine, driver potentials occurred spontaneously in some preparations. In TEA these were not regular in rate. In procaine, spontaneity and its regularity increase at higher concentrations, being consistently present and regular at 7 mM. The effect of alterations of [Ca]o on driver potential responses in the presence of TTX + TEA was examined. Reduction of [Na]o leads to driver potential responses of increased peak amplitude and rates of rise and fall, relative to those in normal Na TTX-TEA. In the presence of TTX and 4 mM Mn, membrane depolarization in response to depolarizing current shows droop after about 50 ms provided depolarization reaches a value of -30 mV. Perfusion with TTX-K-free saline leads to hyperpolarization of approximately 10 mV. The observations are consistent with the following mechanisms for generation of driver potentials: a voltage-dependent conductance increase to Ca leads to regenerative depolarization if the membrane is depolarized sufficiently to produce inward current in excess of outward. The observed peak amplitude is limited by development, in response to depolarization, of increased outward conductance and perhaps by electrotonic decrement from a site distant from the soma. Repolarization occurs by a voltage-dependent K conductance increase and may also include a Ca-dependent K conductance increase. The inhibition of driver potentials by 4 mM Mn and the observation that bursting in the non-TTX-treated, spontaneously active ganglion is eliminated by 4 mM Mn support the suggestion that driver potentials represent the mechanism responsible for organization of neuronal impulse firing into bursts in cardiac ganglia.