Calcium currents in the normal adult rat sympathetic neurone

. The calcium currents evoked by membrane depolarization in the mature and intact rat sympathetic neurone have been studied at 37 degrees C using two-electrode voltage-clamp analysis. 2. Under conditions that eliminate Na+ and K+ currents and 5 mM-external Ca2+, inward currents were observed that activated at about -30 mV and reached maximum amplitude between 0 and +10 mV with time-to-peak values (2.7-1.9 ms) decreasing with increasing membrane depolarization. Thereafter, calcium current (ICa) decayed to a virtually zero level with maintained depolarization. Two exponentials were required to describe the total inactivation process. The faster rate (tau = 29.3-17.6 ms) is ten times the slower rate and proved to be only slightly voltage-dependent. Double-pulse experiments gave a similar time course of turn-off. 3. No steady-state inactivation was removed at holding potentials between -40 and -70 mV and indirect data suggest that all the ICa was available at -50 mV. Within the -30 to -50 mV holding potential range no significant modifications either in the final amount of ICa inactivation or in the inactivation time constant values were detected. 4. After an initial 100 ms, recovery from inactivation followed a single-exponential process with a mean time constant value of 1.54 s at -50 mV. 5. The kinetics of ICa observed in this neurone were consistent with the existence of a single class of Ca2+ channels. For times up to 20 ms, ICa is described reasonably well by a Hodgkin-Huxley c2hc scheme. The activation time constant was 0.57 ms close to threshold and 0.29 ms at +30 mV. Deactivation occurred with a similar fast time course. The steady-state value of the variable c was evaluated in the -40 to +20 mV voltage range: 9.9 mV are required to change c infinity e-fold. 6. Following previous analyses, we have formulated a mathematical model which incorporates the present ICa kinetic equations with Hodgkin-Huxley-type gating mechanisms for INa, IA and IK(V) conductances. The Ca2+ load of the neurone proved to be basically an 'off' effect and to be governed by the duration of the action potential falling phase. The model is consistent with the experimental observations indicating that Ca2+ channels probably do not have an important direct electrical function in the sympathetic neurone spike at normal membrane potential levels.(ABSTRACT TRUNCATED AT 400 WORDS)