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  • Title: Block of avian cardiac fast sodium channels by tetrodotoxin is enhanced by repetitive depolarization but not by steady depolarization.
    Author: Inoue D, Pappano AJ.
    Journal: J Mol Cell Cardiol; 1984 Oct; 16(10):943-52. PubMed ID: 6096567.
    Abstract:
    The blockade of Na+ channels by tetrodotoxin (TTX) was studied in the avian heart with the maximum rate of rise (Vmax) of phase 0 of the action potential used as an indicator of Na+ conductance (gNa). Inhibition by TTX of Vmax occurred at lower concentrations (IC50 congruent to 20 nM) than those reported in mammalian hearts (IC50, 1 to 10 microM). The IC50 was not affected by K+-induced membrane depolarization. Inhibition of closed Na+ channels by TTX was demonstrated and the degree of inhibition was increased by repetitive excitation. The time constant for recovery (tau Rec) from inactivation of Vmax was increased by TTX, a result consistent with the ability of the toxin to trap Na+ channels in the inactivated state. Reduction of the external Na+ concentration [( Na+]0 by 50% reduced the IC50 5.3-fold. This shift can largely be accounted for by the non-linear relationship between Vmax and gNa, that is, there need not be an important effect of [Na+]0 on toxin binding to its receptor. The interaction between TTX and its receptor in the avian heart is about as sensitive as that observed in peripheral nerve. However, like its less-sensitive mammalian heart counterpart, the TTX-Na+ channel interaction is frequency-dependent and apparently little influenced by membrane voltage or [Na+]0.
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