Activation of a nonspecific cation conductance by intracellular Ca2+ elevation in bursting pacemaker neurons of Helix pomatia.
The pacemaker current of a bursting neuron of Helix pomatia was investigated using voltage-clamp and pressure-injection techniques. In the steady state the net membrane current was zero near threshold of the action potential at -45 mV. Negative to this potential the membrane current was inward and steady. During burst activity a long-lasting inward current instantaneously appeared with voltage steps to membrane potentials below -20 mV. This inward current was already present when the clamp step fell into the rising phase of the first spike and became larger during the depolarizing phase of the spike. The repolarization phase and the interspike interval did not add much current. As the spike duration became longer in the course of the burst discharge the inward current grew in amplitude, but its increase was not proportional to that of the spike duration. This was observed with clamp steps to the potassium equilibrium potential (EK = -70 mV). The inward current decayed during a hyperpolarizing step with a half time of approximately 400 ms, which was invariant to voltage as measured between -40 and -100 mV. It decreased linearly from -100 to -40 mV with an extrapolated zero potential of about -20 mV. The inward current was not generated by spikes if the Ca2+ conductance was blocked by Ni2+. At membrane potentials positive to EK the development of an outward current, probably carried by K+, could be observed during the burst. It overlasted the inward current and decayed with time constants of 6-7 s. This current grew successively in amplitude in the course of the burst discharge and finally nullified the inward-current component at potentials around spike threshold, thus terminating the burst. An inward current with properties similar to the spike-induced inward current was produced by pressure injecting CaCl2 into the neurons. This current was unselectively carried by cations as shown by both ion-substitution experiments and measurements with ion-selective microelectrodes. Large cations such as choline, TEA, and Tris passed through the channels nearly as well as Na+. Changes in the H+ or Cl- concentration were not seen to affect the inward current. Spike as well as the injection-induced currents were largest in bursting pacemaker cells compared with other cells of similar size. Both currents were found to be small or absent in nonbursting but regularly firing pacemaker cells, albeit these cells reveal a larger Ca2+ current density than the bursting pacemaker cell.(ABSTRACT TRUNCATED AT 400 WORDS)
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D000200:Action Potentials; D000818:Animals; D002118:Calcium / Q000378:metabolism* / Q000494:pharmacology / Q000502:physiology; D004553:Electric Conductivity; D005724:Ganglia / Q000502:physiology; D006372:Helix, Snails; D007424:Intracellular Fluid / Q000378:metabolism / Q000502:physiology; D007473:Ion Channels / Q000378:metabolism / Q000502:physiology*; D009431:Neural Conduction / Q000187:drug effects*; D009474:Neurons / Q000502:physiology*; D011930:Reaction Time / Q000502:physiology; D012964:Sodium / Q000494:pharmacology
D007473:Ion Channels; D012964:Sodium; D002118:Calcium