Electrical properties of a cockroach motor neuron soma depend on different characteristics of individual Ca components

The ''fast'' coral depressor motor neuron (D-f) of the cockroach is among the most extensively studied of insect neurons. It has been shown that the cell body of this neuron can exhibit active electrical properties, which may change over time or with chemical modulation. To further understand these electrical events and their modulation, inward currents in D-f have been characterized under conditions in which outward currents have been suppressed. The inward current activated at potentials positive to -60 mV and peaked between -10 and 0 mV when measured in barium saline and between 0 and +10 mV when measured in calcium saline. The inward current was insensitive to Ni2+ (100 mu M) but reduced by verapamil (50 mu M) and abolished by Cd2+ (1 mM). Two components of I-Ca were identified by their sensitivity to either 50 mu M nifedipine or micromolar Cd2+ The nifedipine-sensitive component activated positive to -60 mV and peaked between -10 and 0 mV, whereas the Cd2+-sensitive component activated positive to -40 mV and peaked between +10 and +20 mV. Immediately after dissection, depolarization of D-f evoked plateau potentials, whereas 1-4 h after dissection, depolarization evoked action potentials. The plateau potentials were insensitive to 100 mu M Cd2+ but blocked by 50 mu M nifedipine, whereas the spikes required a combination of nifedipine (50 mu M) and Cd2+ (100 mu M) for complete suppression, indicating that only one component of I-Ca contributes to the plateau potential, whereas both components contribute to action potentials. Currents measured in calcium saline decayed faster than currents measured in barium saline. The inactivation characteristics were investigated with the use of double-pulse voltage-clamp experiments. I(Ca)showed a greater degree of inactivation and slower recovery from inactivation than did I-Ba Current decay and the extent of inactivation were reduced after injection of the calcium-chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA). This suggests that the calcium current of this neuron displays calcium-dependent inactivation. An additional mechanism, most probably voltage-dependent inactivation, also occurs because I-Ba, even in neurons injected with BAPTA, displayed some inactivation. The inactivation characteristics may be important in determining activity displayed by D-f. Indirect evidence suggests that intracellular calcium is high immediately after dissection. At this time, the calcium current may therefore be reduced due to calcium-dependent inactivation. This may, at least partly, explain why the cell does not spike shortly after dissection.