title: Effect of calcium and calcium channel blockers on transient outward current of F76 and D1 neuronal soma membranes in the subesophageal ganglia of Helix aspersa.
abstract: Twin-electrode voltage-clamp techniques were used to study the effect of calcium and calcium channel blockers on the transient outward current in isolated F76 and D1 neurones of Helix aspersa subesophageal ganglia in vitro (soma only preparation with no cell processes). On lowering extracellular Ca(2+) concentration from 10 to 2 mm or removing extracellular calcium from the bathing medium, the threshold for this current shifted in a negative direction by 11. 5 and 20 mV, respectively. On the other hand, increasing the extracellular Ca(2+) concentration from 10 to 20 and to 40 mm shifted the steady-state inactivation curves in positive directions on the voltage axis by 7 and 15 mV, respectively. Upon application of calcium channel blockers, Co(2+), La(3+), Ni(2+) and Cd(2+), transient potassium current amplitude was reduced in a voltage-dependent manner, being more effective at voltages close to the threshold. The current was elicited even at a holding potential of -34 mV. The specific calcium channel blockers, amiloride and nifedipine did not shift the activation and steady-state inactivation curves and did not reduce the transient outward current amplitude. It was concluded that the transient outward current is not dependent on intracellular Ca(2+) but that it is modulated by Ca(2+) and di- and trivalent ions extracellularly. The effects of these ions are very unlikely to be due to a surface charge effect because the addition of La(3+) (200 microm) completely reverses the shift in a hyperpolarizing direction when the extracellular Ca(2+) concentration was reduced from 10 to 1 mm and additionally shifts the kinetics further still in a depolarizing direction. The responses seen here are consistent with a specific effect of di- and trivalent ions on the transient outward current channels leading to a modification of gating.
authors.affiliation: Department of Physiology, University Medical School, Newcastle Upon Tyne, NE2 4HH, UK.
authors.forename: R
authors.initials: R
authors.lastname: Bal
authors.forename: M
authors.initials: M
authors.lastname: Janahmadi
authors.forename: G G
authors.initials: GG
authors.lastname: Green
authors.forename: D J
authors.initials: DJ
authors.lastname: Sanders
mesh_terms: D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000494:pharmacology*; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D017952:Ganglia, Invertebrate / Q000187:drug effects*; D006372:Helix, Snails / Q000502:physiology*; D007700:Kinetics; D008670:Metals / Q000494:pharmacology; D009543:Nifedipine / Q000494:pharmacology; D009994:Osmolar Concentration; D018408:Patch-Clamp Techniques
chemical_list: D002121:Calcium Channel Blockers; D008670:Metals; D000584:Amiloride; D009543:Nifedipine; D002118:Calcium