Slow inactivation of sodium currents in the rat nodose neurons

• Published in: Autonomic neuroscience 2001-03, Vol.87 (2), p.209-216
• Main Authors: Fazan, Rubens, Whiteis, Carol A., Chapleau, Mark W., Abboud, Francois M., Bielefeldt, Klaus
• Format: Article
• Language: English
• Subjects: Action Potentials - drug effects; Action Potentials - physiology; Animals; Biological and medical sciences; Cumulative inhibition; Fundamental and applied biological sciences. Psychology; Ion Channel Gating - drug effects; Ion Channel Gating - physiology; Male; Neural Inhibition - physiology; Neurons, Afferent - physiology; Nodose Ganglion - cytology; Patch-Clamp Techniques; Peripheral nervous system. Autonomic nervous system. Neuromuscular transmission. Ganglionic transmission. Electric organ; Rats; Rats, Sprague-Dawley; Sensory neurons; Sodium - metabolism; Sodium Channels - metabolism; Sodium currents; Tetrodotoxin - pharmacology; Vertebrates: nervous system and sense organs
• ISSN: 1566-0702; 1872-7484
• DOI: 10.1016/S1566-0702(00)00281-2

Nodose neurons express sodium currents that can be differentiated based on their sensitivity to tetrodotoxin. Several studies have demonstrated significant differences in voltage-dependence and kinetics of activation and inactivation between tetrodotoxin-sensitive and tetrodotoxin-resistant currents. However, little is known about the slow inactivation. Using whole cell patch-clamp technique fast and slow inactivation of sodium currents were studied in cultured rat nodose neurons. Tetrodotoxin-resistant currents recovered much more rapidly after a 15-ms depolarization than tetrodotoxin-sensitive currents. However, repeated 5-ms depolarizations at 10 Hz induced a cumulative inhibition that was more prolonged in tetrodotoxin-resistant compared to tetrodotoxin-sensitive currents. Consistent with these findings, slow inactivation proceeded more rapidly and was more complete for the tetrodotoxin-resistant than for tetrodotoxin-sensitive currents. While the voltage-dependence of fast inactivation differed significantly between the pharmacologically distinct currents, the voltage-dependence of slow inactivation was similar for both sodium currents. We conclude that slow inactivation of sodium currents can be triggered by trains of brief depolarizations. The resulting prolonged decrease in membrane excitability may contribute to the different patterns of action potential generation observed in primary afferent neurons.