Ionic conductance associated with electrical activity of guinea‐pig red nucleus neurones in vitro.
Masaya Kubota, Makoto Nakamura, N. Tsukahara
Abstract
Masaya Kubota, Makoto Nakamura, N. Tsukahara
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.
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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.
Key concepts: Tetraethylammonium, Depolarization, Tetrodotoxin, Biophysics, Hyperpolarization (physics), Chemistry, Conductance, Membrane potential