Immobilization of intramembrane charge in Myxicola giant axons.

Bullock, J.O.; Schauf, C. L.

doi:10.1113/jphysiol.1979.sp012611

Cited by 27 publications

(14 citation statements)

References 13 publications

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“…Similar results have been reported for crayfish giant axons (Swenson, 1980), frog node of Ranvier (Nonner, 1980), and frog skeletal muscle (Campbell, 1983). However, a lack of correlation between charge immobilization and INa inactivation has been reported in squid (Meves and Vogel, 1977) and Myxicola (Bullock and Schauf, 1979) giant axons. In the present report we found that the value of %, measured from the decay of INa during maintained depolarizations, varied by as much as a factor of 3 among patches at the same potential (Table III), and no systematic difference in *h was observed between cell-attached and inside-out patches.…”

Section: Discussionsupporting

confidence: 86%

Patch recordings from the electrocytes of electrophorus. Na channel gating currents.

Shenkel

Bezanilla

1991

The Journal of General Physiology

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A B S T R ACT Gating currents were recorded at 1 I°C in cell-attached and inside-out patches from the innervated membrane of Electrophorus main organ electrocytes.With pipette tip diameters of :3-8 v~m, maximal charge measured in patches ranged from 0.74 to 7.19 fC. The general features of the gating currents are similar to those from the squid giant axon. The steady-state voltage dependence of the ON gating charge was characterized by an effective valence of 1.3 -+ 0.4 and a midpoint voltage of -56 -+ 7 inV. The charge vs. voltage relation lies ~30 mV negative to the channel open probability curve. The ratio of the time constants of the OFF gating current and the Na current was 2.3 at -120 mV and equal at -80 mV. Charge immobilization and Na current inactivation develop with comparable time courses and have very similar voltage dependences. Between 60 and 80% of the charge is temporarily immobilized by inactivation.

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Section: Discussionsupporting

confidence: 86%

Patch recordings from the electrocytes of electrophorus. Na channel gating currents.

Shenkel

Bezanilla

1991

The Journal of General Physiology

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“…The decline in TOFF with pulse durations that would have produced significantly increasing sodium inactivation has been previously observed in both squid axons (Fig . 2 of Armstrong and Bezanilla, 1977) and node of Ranvier (Nonner et al ., 1978 ;Nonner, 1980), but not in Myxicola axons (Table I of Bullock and Schauf, 1979) . These comparisons seem to indicate that the sodium channel gating processes may be similar in squid and frog axons, at least insofar as can be determined from gating charge movement measurements, but that both may differ from the gating process in Myxicola axons.…”

Section: Comparison With Previous Observationsmentioning

confidence: 95%

Kinetics of intramembrane charge movement and sodium current in frog node of Ranvier.

Dubois¹,

Schneider²

1982

The Journal of General Physiology

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Intramembrane charge movement (Q) and sodium current (IN.) were monitored in isolated voltage-clamped frog nodes of Ranvier. ON charge movements (QON) for pulses from the holding potential (-100 mV) to potentials V :f:-:0 mV followed single exponential time courses, whereas two exponentials were found for pulses to V ?20 mV. The voltage dependence of both QON and its time constant TON indicated that the two ON components resolved at V ?20 mV were also present, though not resolvable, for pulses to V<0 MV. OFF charge movements (QOFF) monitored at various potentials were well described by single exponentials . When QOFF was monitored at -30 or -40 mV after a 200-tt,s pulse to +20 mV and QON was monitored at the same potential using pulses directly from -100 mV, TON/,rOFF = 2.5 t 0.3. At a set OFF potential (-90 to -70 mV), TOFF first increased with increasing duration ION of the preceding pulse to a given potential (0 to +30 mV) and then decreased with further increases in ION . The declining phase of TOFF followed a time course similar to that of the decline in QOFF with ION . For the same pulse protocol, the OFF time constant TN. for IN. also first increased with ION but then remained constant over the ION interval during which TOFF and QOFF were declining. After 200-or 300-us pulses to +20, +30, or +50 mV, TOFF/TN . at -70 to -90 mV was 1 .2 t 0.1 . Similar TOFF/TN . ratios were predicted by channel models having three identical charged gating particles that can rapidly and reversibly form an immobile dimer or trimer after independently crossing the membrane from their OFF to their ON locations.

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“…Independently of whether the inactivation blocking site is a component of the normal gating machinery or not, it is clear that if some fraction of resting channels have this site occupied, by e.g., K, then these channels inherently have inactivation coupled to activation in that a conducting channel is necessary to clear the sites and so permit the inactivation gates to close. The nature of the coupling between activation and inactivation certainly involves more just this effect, however, as immobilization of the gating charge (Armstrong and Bezanilla, 1977;Meves and Vogel, 1977;Neumcke et al, 1976;Nonner et al, 1978;Nonner, 1980;Bullock and Schauf, 1979;Swenson, 1980;Starkus et al, 1981) establishes that the operation of the activation gates is itself dependent on the inactivation state of the channel, and because channels can also inactivate without conducting (Gillespie and Meves, 1980;Bean, 1981;Horn et al, 1981;Aldrich et al, 1983;Horn and Vandenberg, 1984). I thank Drs.…”

Section: A Possible Mechanism For Inactivationmentioning

confidence: 99%

Internal cesium and the sodium inactivation gate in Myxicola giant axons

Goldman¹

1986

Biophysical Journal

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Internal cesium (CSi), relative to internal potassium (Ki), alters Na current (INa) time course in internally perfused Myxicola giant axons. CSi slows the time to peak INa, slows its decline from peak and increases the steady state to peak current ratio, INainfinity/INapeak. Neither activation nor deactivation kinetics are appreciably affected by CSi. Na current rising phases, times to half maximum and tail current time courses are similar in CSi and Ki. Inactivation time constants determined by both one (tau h) and two (tau c) pulses are also little changed by CSi. The CSi effects are due largely or entirely to an increased INainfinity/INapeak. CSi decreases the steady level of inactivation reached during a step in potential, preventing some fraction of inactivation gates from closing at all, the rest apparently closing normally. Inactivation block in CSi decreases with increasing inward current magnitude and in Ki inactivation block is appreciable only for outward Na channel current, suggesting the site of action is located somewhere in the current pathway. If this site mediates the normal operation of the inactivation gate, then a possible mechanism for gate closure could involve a positively charged structure moving to associate with a negative site near or into the inner channel mouth.

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Immobilization of intramembrane charge in Myxicola giant axons.

Abstract: [15][16][17][18][19][20] mV from the normalized Na inactivation curve.

Cited by 27 publications

References 13 publications

Patch recordings from the electrocytes of electrophorus. Na channel gating currents.

Patch recordings from the electrocytes of electrophorus. Na channel gating currents.

Kinetics of intramembrane charge movement and sodium current in frog node of Ranvier.

Internal cesium and the sodium inactivation gate in Myxicola giant axons

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