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  • Title: Action of benzocaine on sodium channels of frog nodes of Ranvier treated with chloramine-T.
    Author: Meeder T, Ulbricht W.
    Journal: Pflugers Arch; 1987 Jul; 409(3):265-73. PubMed ID: 2442701.
    Abstract:
    Single myelinated nerve fibres of the frog Rana esculenta were voltage clamped in solutions containing 10 mM TEA to block potassium channels. Reduction of peak INa was measured after equilibrating the membrane in solution containing benzocaine between 0.025 and 2.0 mM. A Hill plot of this effect revealed a slope nH approximately 1 between 0.25 and 1.0 mM but showed deviations for the lowest concentrations (nH less than 1) and the highest concentration (nH greater than 1). Treatment with 0.6 mM chloramine-T irreversibly partially inhibited inactivation of sodium channels leading to a large INa component persisting during depolarization. After treatment the benzocaine effect on peak INa (tested with 0.25-1.0 mM) was unchanged but the persistent component was much more depressed. Benzocaine shifted the steady-state inactivation curve to more negative potentials. This was also observed after chloramine-T treatment which itself produced a curve of decreased slope, shifted to more positive potentials. Recovery from inactivation was studied at different levels of hyperpolarization; it was diphasic in anaesthetic-free solutions before and after chloramine-T treatment although slowed in the latter case. In benzocaine recovery started with a delay (less than 0.6 ms at 16-18 degrees C) and proceeded with a single time constant that decreased with increasing hyperpolarization, was independent of benzocaine concentration and not affected by chloramine-T. The results are compatible with the idea that the affinity of the binding site for benzocaine increases when the channel state changes from resting to open to inactivated with equilibrium dissociation constants of the reaction with resting channels, KR = 0.7 mM and with inactivated channels, KI = 0.04 mM.(ABSTRACT TRUNCATED AT 250 WORDS)
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