EFFECTS OF CA2-PIG POSTGANGLIONIC SYMPATHETIC-NERVE TERMINALS( AND K+CHANNEL BLOCKERS ON NERVE IMPULSES RECORDED FROM GUINEA)

1. A focal extracellular suction electrode was used to investigate the contributions of K+ and Ca2+ currents to the nerve impulse recorded f rom sympathetic nerve terminals innervating the guinea-pig vas deferen s in vitro. 2. Perfusing the electrode with Cd2+ (0.1-0.5 mM) had litt le effect on tile configuration of the nerve impulse. 3. Perfusing the electrode with Ba2+ (1-3 mM) caused the appearance of a second negati ve-going component of the nerve impulse. Local application of Cd2+ (0. 1 mM) had little affect on this component of the nerve impulse. 4. Per fusing the electrode with 4-aminopyridine (4-AP) and/or tetraethylammo nium (TEA) caused the appearance of a second negative-going component of the nerve impulse. This component has been termed the late negative -going component (LNC). 5. The LNC produced by local application of 1 mM 4-AP and 10 mM TEA was not changed when the solution perfusing tile electrode contained no added Ca2+, 10 mM Ca2+ or omega-conotoxin GVIA (0.1 mu M). Perfusion of the electrode with Cd2+ (0.1 mM) reduced the amplitude and slowed the time course of the LNC. 6. The LNC was marke dly inhibited when the organ bath was perfused with TEA (10 mM) or 4-A P and TEA (1 and 10 mM, respectively). In some experiments the LNC was completely abolished. 7. The LNC was reduced in amplitude and slowed in time course when the solution perfusing the organ bath contained no added Ca2+. A similar effect on the LNC was observed when the solutio n perfusing the organ bath contained omega-conotoxin GVIA (0.1 mu M), charybdotoxin (0.05 mu M) or low concentrations of TEA (0.3-1 mM) or B a2+(10-500 mu M). 8. Bath application of the alpha(2)-adrenoceptor ago nist clonidine (0.1-0.3 mu M) did not detectably change the LNC. 9. Th e results demonstrate that the LNC produced by the local application o f K+ blockers is due primarily to K+ efflux from sites outside the rec ording electrode and that a part of the change in conductance that und erlies this component is due to opening of Ca2+-activated K+ channels. The failure to detect an effect of clonidine on the LNC suggests that activation of presynaptic alpha(2)-adrenoceptors does not change eith er the K+ or the Ca2+ conductance of the nerve terminals.