A CALCIUM-DEPENDENT COMPONENT OF THE ACTION-POTENTIAL IN SYMPATHETIC-NERVE TERMINALS IN RAT TAIL ARTERY

A pharmacological approach was employed in order to visualize a Ca2+-dependent component of the extracellularly recorded nerve terminal impulse in the secretory regions of the sympathetic postganglionic nerves in the rat tail artery. Application of potassium-channel-blocking agents within the recording electrode caused the nerve terminal impulse to acquire a delayed negative deflection, which we have termed the late negative component (LNC) of the nerve terminal impulse. The time course and the latency of the LNC differed from that of the postjunctional transmitter-induced excitatory junction current, and the LNC persisted when the excitatory junction current was blocked by adenosine [alpha-beta-methylene] triphosphate, and was resistant to the alpha-1-antagonist prazosin and the alpha-2-antagonist yohimbine. Probably, therefore, the LNC was exclusively prejunctional in origin. For the following reasons it seems likely that the LNC, at least in part, was caused by influx of Ca2+ into the secretory regions of these nerves: (a) the LNC occured only when potassium-blocking agents were present within the recording electrode; (b) the LNC amplitude increased with the Ca2+ concentration inside the recording electrode and was reduced by the removal of Ca2+; (c) the LNC was enhanced by replacing Ca2+ in the medium inside the recording electrode with Ba2+; (d) the LNC was depressed by the inorganic Ca2+-channel blocker cadmium or the Ca2+ -channel-blocking peptide omega-conotoxin added within the recording electrode only, or by addition of cadmium or cobalt (but not the organic Ca2+-channel blocker nifedipine) inside and outside the recording electrode. In our opinion, these lines of evidence indicate that the LNC represents at least in a part a Ca2+-dependent component of the nerve terminal impulse in the secretory regions of these nerves. The extent to which the LNC can be used as a quantitative measure of nerve-impulse-induced influx of Ca2+ into the nerve terminals remains to be established.