Effects of veratridine on single neuronal sodium channels expressed in Xenopus oocytes.
(1) Chick neuronal Na+ channels were expressed in Xenopus laevis oocytes after injection with total messenger ribonucleic acid (mRNA) isolated from chick brain. The currents were investigated with the whole cell voltage clamp and with the patch clamp technique. Activation and inactivation of the induced current, and its sensitivity towards tetrodotoxin (TTX) and veratridine were reminiscent of vertebrate neuronal Na+ channels. (2) In the presence of veratridine normal single channel openings often converted into small amplitude openings of long duration. These small amplitude openings persisted for hundreds of milliseconds after return to the holding potential. (3) The slope conductance of the veratridine modified open channel state was 5-6 pS as compared to the normal state with 21-25 pS in the voltage range between -35 and +5 mV. (4) The modified channel showed saturation behaviour towards Na+ ions. Half saturation of the single channel amplitude was observed at 330 mM Na+ at a membrane potential of -100 mV. (5) Final closure of the modified channel after return to the holding potential followed an exponential time course. Its potential dependence was similar to that of the time course of the veratridine induced tail currents in the whole cell configuration. (6) The properties of the Na+ channel derived from chick forebrain are compared with the properties of the same channel derived from chick skeletal muscle. Both were expressed in the same membrane environment, the Xenopus oocyte plasma membrane. While earlier results with Na+ channels of muscle origin showed two channel populations, one with short and another with long mean open times, Na+ channels of neuronal origin were homogeneous and characterized by short open times.
D000818:Animals; D001921:Brain / Q000502:physiology; D002645:Chickens; D066298:In Vitro Techniques; D007473:Ion Channels / Q000187:drug effects*; D008564:Membrane Potentials; D009132:Muscles / Q000502:physiology; D009474:Neurons / Q000187:drug effects*; D009865:Oocytes; D012333:RNA, Messenger / Q000502:physiology; D012964:Sodium / Q000378:metabolism*; D014701:Veratridine / Q000494:pharmacology*; D014702:Veratrine / Q000031:analogs & derivatives*; D014982:Xenopus laevis
D007473:Ion Channels; D012333:RNA, Messenger; D014701:Veratridine; D012964:Sodium; D014702:Veratrine