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

Abstract

SUMMARY1. Depolarizing voltage-clamp pulses elicit a triphasic series of tail currents (phase I, II and III) in Aplysia burst-firing neurones L2-L6. The sequence and time course of the tail currents resemble slow changes in membrane potential which follow bursts in the unclamped cell.2. The phase II tail current is an inward current with a time course similar to that of the depolarizing after-potential (d.a.p.) which follows bursts in the unclamped cell.The phase II tail current is suppressed by depolarizing pulses which approach Eca, is blocked by Ca2+ current antagonists (Co2+ and Mn2+), and is blocked by intracellular injection of EGTA.3. The phase II tail current is not blocked by agents which block Na+-dependent action potentials, the Na+{-Ca2+ exchange pump, or the Na+-K+ exchange pump. The phase II tail current is not blocked by the elimination of large outward K+ currents which can lead to extracellular K+ accumulation. Thus, the phase II tail current is not generated by any of these processes.4. The phase II tail current is reduced by about 60 % following substitution of tetramethylammonium (TMA+) for external Na+, but is unaffected by reducing external Cl-.5. The phase II tail current is distinct from a persistent inward Ca2+ current which underlies the negative resistance region of the steady-state current-voltage relation of bursting cells. The persistent inward current is only slightly reduced by TMA+ substitution for Na+, and is enhanced by EGTA injection.6. Injection of Ca2+ into Aplysia bursting cells elicits a biphasic (inward-outward)current. The inward current can be observed in isolation after blocking the outward component (Ca2+-activated K+ current) with 50 mM-external tetraethylammonium. 7. The Ca2+-elicited inward current has a reversal potential near -22 mV, and is non-selective for Na+, K+ and Ca2+. The reversal potential is unaffected by changes in Cl-and pH. The Ca2+-activated conductance is apparently voltage independent.8. We propose that the phase II tail current, and hence the d.a.p., is due to the Ca2+-dependent activation of a voltage-independent non-specific cationic conductance. This conductance participates in generating the depolarizing phase of bursting pace-maker activity.

Reduced outward K+ conductances generate depolarizing after–potentials in rat supraoptic nucleus neurones

“…The DAPs last for hundreds of milliseconds to seconds and have amplitudes up to 10 mV, depending on the number of preceding spikes and membrane potential levels at which they are evoked (Andrew & Dudek, 1984;Andrew, 1987). Resembling those identified in invertebrate bursting pacemaker neurones (Thompson & Smith, 1976;Kramer & Zucker, 1985a) and other mammalian CNS neurones (Llin as, 1988;White, Lovinger & Weight, 1989), DAPs as well as phasic firing in SON neurones are abolished by depleting extracellular Ca¥, blocking membrane Ca¥ channels or chelating cytosolic free Ca¥ (Inenaga, Akamatsu, Nagatomo, Ueta & Yamashita, 1992;Li et al 1995). Our recent study has further demonstrated that interference with Ca¥-induced Ca¥ release from internal stores, with either blockade of intracellular ryanodine receptors or depletion of internal Ca¥ pools, reduces DAPs and eliminates phasic firing in SON cells (Li & Hatton, 1997).…”

Dendritic Control of Spontaneous Bursting in Cerebellar Purkinje Cells

“…In each of these cases, activation of the calcium channels contributes a depolarizing current that helps bring the cell to threshold during the bursts. Bursts are terminated by inactivation of the calcium channels (Kramer and Zucker, 1985;Huguenard and Prince, 1992;Bal and McCormick, 1997) or by activation of calciumactivated potassium channels after calcium entry (Wong and Prince, 1978;Del Negro et al, 1999;Golding et al, 1999). In Purkinje neurons, however, P/Q-type calcium channels are responsible for the abrupt termination of each burst by generating a dendritic calcium spike.…”

Ca(2+)‐dependent inactivation of Ca2+ current in Aplysia neurons: kinetic studies using photolabile Ca2+ chelators.

“…Details of the ganglion removal, desheathing, axotomy and solution changes have been previously described (Kramer & Zucker, 1985; Lando & Zucker, 1989). Most experiments were done on axotomized left upper quadrant neurons, particularly L3 and L6 which have been shown to possess a Ca2+-activated K+ conductance (IK(ca)) that is largely abolished by extracellular tetraethylammonium (TEA+) ions (Deitmer & Eckert, 1985).…”

“…Details of the two-electrode voltage clamp technique employed have been previously described (Smith & Zucker, 1980; Kramner & Zucker, 1985). In all Ica experiments, the voltage and current electrodes were filled with 3 M CsCl and had resistances of 1-5 MCI.…”