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BarbituratesBlockSodiumand.PDF
Barbiturates Block Sodium and
Potassium Conductance Increases in
Voltage-Clamped Lobster Axons
M. P. BLAUSTEIN
From the Naval Medical Research Institute, Bethesda, Maryland 20014. Dr. Blausteins
present address is Department of Physiology, Cambridge University, England
ABSTRACT Sodium pentobarbital and sodium thiopental decrease both the
peak initial (Na) and late steady-state (K) currents and reduce the maximum
sodium and potassium conductance increases in voltage-clamped lobster giant
axons. These barbiturates also slow the rate at which the sodium conductance
turns on, and shift the normalized sodium conductance vs. voltage curves in
the direction of depolarization along the voltage axis. Since pentobarbital
(pK, = 8.0) blocks the action potential more effectively at pH 8.5 than at pH
6.7, the anionic form oi the drug appears to be active. The data suggest that
these drugs affect the axon membrane directly, rather than secondarily through
effects on intermediary metabolism. It is suggested that penetration of the lipid
layer of the membrane by the nonpolar portion of the barbiturate molecules
may cause the decrease in membrane conductances, while electrostatic inter-
actions involving the anionic group on the barbiturate, divalent cations, and
fixed charges in the membrane could account for the slowing of the rate of
sodium conductance turn-on and the shift of the normalized conductance curves
along the voltage axis.
INTRODUCTION
It is now well-established that the local anesthetic, procaine, blocks the nerve
action potential by reducing both the early transient (Na) and late steady-
state (K) conductance increases in the isolated peripheral nerve fiber (Taylor,
1959; Shanes et al., 1959; and Blaustein and Goldman, 1966 a). Similar
effects are observed in the perfused squid axon whether procaine is applied
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