Abstract
Intracellular recordings were made from red nucleus (r.n.) neurones in guinea-pig slice preparations in vitro. In the control solution, a fast action potential was elicited by a depolarizing current pulse. This fast action potential was abolished by tetrodotoxin (TTX). When tetraethylammonium (TEA) was added to the perfusing solution, a TTX-resistant slow action potential was elicited by a large depolarizing current pulse. This TTX-resistant slow action potential was abolished by Co2+ or Mn2+. In the control solution, the action potential was followed by a fast and a slow after-hyperpolarization (a.h.p.). The fast a.h.p. was abolished by TEA. The amplitude of the fast a.h.p. was dependent on the extracellular K+ concentration. The slow a.h.p. was reversibly abolished by Co2+ or Mn2+. The reversal potential of the slow a.h.p. was dependent on the extracellular K+ concentration. When the membrane potential was hyperpolarized, a time-dependent inward rectification was observed. This inward rectification was inhibited by Cs+ but not by Ba2+, TTX, TEA or Co2+. It is concluded that the fast action potential is produced by a voltage-dependent Na+ conductance, the TTX-resistant slow action potential is produced by a voltage-dependent Ca2+ conductance, the fast a.h.p. is produced by a voltage-dependent K+ conductance, the slow a.h.p. is produced by a Ca2+-activated K+ conductance and the inward rectification is produced by a time-dependent inward rectifier in r.n. neurones.