A voltage‐sensitive persistent calcium conductance in neuronal somata of Helix.

Abstract

SUMMARY1. An intracellular voltage clamp in conjunction with a patch pipette utilizing feed-back to monitor local current from the soma membrane were used to analyse transient and stationary currents in bursting pacemaker neurones in Helix pomatia and H. levantina.2. A weak, net inward current flows during small (< 20 mV) depolarizations. This current exhibits slow activation kinetics, persistence during prolonged depolarization, and slow turning off at end of depolarization. Consequently, the steady-state current-voltage curve exhibits a region of negative resistance from about -55 to -35 mV.3. The slow inward current and the negative resistance characteristic are rapidly and -completely abolished by substitution of C02+ or La3+ for Ca2+ and are partially blocked by the Ca-blocking drug D-600. Substitution of Tris or glucose for Na+ significantly reduces the inward current only after 15-20 min exposure, recovery being equally slow.4. The inward current and the negative resistance characteristic of the I-V curve are greatly enhanced by Ba2+ substitution for Ca2+. This is ascribed in part to Ba2+ carrying current through the slow inward current channels and in part to a suppression of the late K+ current by Ba2+.5. The inward current is also present in many non-bursting neurones but fails to appear as a net inward current due to short circuiting by a leakage current or by the delayed potassium current. In these cells the slow inward current contributes to inward going rectification. Replacement of Ca2+ with Ba2+ enhances the current so as to produce a net inward current during small depolarizations in these neurones.6. It is concluded that the slow inward current is carried primarily by * On leave of absence from the

Calcium‐dependent inward current in Aplysia bursting pace‐maker neurones.

“…Thus, unlike the phase II tail current, the decrease in the persistent inward current which occurs upon Na+ substitution is small, and largely irreversible. Therefore, as in Helix bursting neurones (Eckert & Lux, 1976), it is unlikely that Na+ carries any of the persistent inward current in l.u.q.b. cells, although external Na+ seems to be necessary for its maintenance at normal levels.…”

“…Bursting pace-maker neurones exhibit a persistent inward current which underlies the region of negative slope ('negative resistance region') in the pace-maker potential range of the steady-state I-V curve (Eckert & Lux, 1976).The pace-maker range is the range of voltage through which the membrane potential can slowly oscillate during bursting pace-maker activity (i.e. -50 to -30 mV).…”

“…10 mV) depolarizing pulses from within the pace-maker range. A portion of the persistent inward current exhibits slow activation and deactivation kinetics (Eckert & Lux, 1976;Kramer & Zucker, 1985); thus the phase II tail current could conceivably be due to the slow decay of this current following a large depolarizing pulse. Some important characteristics distinguish the persistent inward current from the phase II tail current.…”

“…The depolarizing phase of bursting activity in these cells is thought to be due to a slow, regenerative inward current. Eckert & Lux (1976) detected a persistent inward current in Helix bursting neurones which exhibits slow activation and inactivation kinetics, and which is carried by Ca2+. This current can be observed most clearly during small (about 10 mV) depolarizing voltage-clamp pulses from a holding potential (Vh) within the pace-maker voltage range (i.e.…”

“…This current can be observed most clearly during small (about 10 mV) depolarizing voltage-clamp pulses from a holding potential (Vh) within the pace-maker voltage range (i.e. -30 to -50 mV), and is responsible for the region of negative slope resistance observed in the late (steady-state) current-voltage relationship of these cells (Eckert & Lux, 1976). A similar negative resistance region has been found in Aplysia bursting pace-maker neurones, and attributed to a slow inward current carried by Ca2+ (Gorman, Hermann & Thomas, 1982), Na+ (Smith, Barker & Gainer, 1975;Carnevale & Wachtel, 1980), or both Ca2+ and Na+ (Johnston, 1976).…”