Acetylcholine suppresses calcium current in neurons of Aplysia californica.
1. The left upper quadrant neurons L2-L6 in the abdominal ganglion of Aplysia californica were voltage clamped in order to examine effects of acetylcholine on voltage-dependent Ca and Ca-dependent K currents. 2. "Puffed" application of 10-100 microM acetylcholine reduced both the early inward and late outward phases of the current elicited by depolarizing voltage steps. An identical effect of the peptide FMRFamide was previously found to result from a suppression of the Ca and Ca-dependent K currents. 3. This effect of acetylcholine was obscured by the simultaneous activation of a previously described K current resembling the "S" current. Extracellular tetraethylammonium (TEA) and 4-aminopyridine could not be used to eliminate this current, because both compounds also appeared to block the acetylcholine receptor mediating the putative suppression of Ca and Ca-dependent K currents. 4. The acetylcholine-induced "S"-like and other K currents could, however, be reduced or eliminated by injection of TEA+ or Cs+ into the cell, replacement of extracellular Ca2+ with Ba2+, and by shifting the K+ equilibrium potential so as to null K currents at the potential used to record Ca current, revealing in each case a partial (10-40%) suppression of the Ca (or Ba) current by acetylcholine. 5. The reduction of the outward phase of depolarization-activated current was confirmed to represent suppression of the Ca-dependent K current by acetylcholine. This effect was indirect, secondary to the suppression of Ca current, since acetylcholine had no effect on Ca-dependent K current elicited by direct injection of Ca2+ into the cell. 6. Activation of the "S"-like K current and suppression of the Ca current by FMRFamide are likely to be important in its proposed role as an agent of presynaptic inhibition in Aplysia. Since acetylcholine has identical effects, it too may have such a function.
Brezina
V
V
Department of Biology, University of California, Los Angeles 90024.
D015761:4-Aminopyridine; D000109:Acetylcholine / Q000037:antagonists & inhibitors / Q000502:physiology*; D000631:Aminopyridines / Q000494:pharmacology; D000818:Animals; D001048:Aplysia / Q000502:physiology*; D001464:Barium / Q000494:pharmacology; D002118:Calcium / Q000502:physiology*; D015220:Calcium Channels / Q000502:physiology; D002800:Cholinesterase Inhibitors / Q000494:pharmacology; D007478:Iontophoresis; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D011188:Potassium / Q000502:physiology; D013757:Tetraethylammonium Compounds / Q000494:pharmacology
D000631:Aminopyridines; D015220:Calcium Channels; D002800:Cholinesterase Inhibitors; D013757:Tetraethylammonium Compounds; D001464:Barium; D015761:4-Aminopyridine; D000109:Acetylcholine; D011188:Potassium; D002118:Calcium