Patch-clamp study of the tetrodotoxin-resistant sodium current in group C sensory neurones.
Conditions were devised to isolate in cranial sensory neurones transfer of Na ions: K and Ca were omitted from the extracellular medium, and simultaneously cells were intracellularly loaded with 120 mM caesium and 20 mM TEA at [Ca]i = 10(-8) M. A tetrodotoxin (TTX)-resistant current was shown to be elicited by step depolarization from -25 MV upwards. This current successively activates and inactivates at increasing rates on further depolarization and at 0 mV (where peak amplitude is reached) its time course is of 20-50 ms. Absence of TTX-sensitivity (up to 15 microM), slow time course and an activation curve shifted by 15 mV towards the depolarized potentials differentiate this current from the more classical fast Na current which can be elicited on the same cells. Inactivation was provoked by a prepulse of varying amplitude and duration: with a prepulse command to -20 mV, inactivation was of 50% within a delay of 300 ms and almost 100% in about 1 min. After complete inactivation by command to 0 mV for 300 ms, recovery by holding the potential at -80 mV was of 50% in 205 ms, and of 100% after 1-4 s. It is concluded that a charge transfer of Na accounts for most of the hump which prolongs the action potential of these sensory neurones, and thus it can be proposed that spike duration as modulated by neurotransmitters may also involve Na in addition to Ca.
D000818:Animals; D003391:Cranial Nerves / Q000378:metabolism*; D046508:Culture Techniques; D004351:Drug Resistance; D005724:Ganglia / Q000378:metabolism; D007473:Ion Channels / Q000378:metabolism*; D009412:Nerve Fibers / Q000378:metabolism; D009620:Nodose Ganglion / Q000378:metabolism; D051381:Rats; D012964:Sodium / Q000378:metabolism*; D013779:Tetrodotoxin / Q000494:pharmacology*
D007473:Ion Channels; D013779:Tetrodotoxin; D012964:Sodium