The effect of temperature on the asymmetrical charge movement in squid giant axons.

Kimura, Jun; Meves, H.

doi:10.1113/jphysiol.1979.sp012748

Cited by 115 publications

(93 citation statements)

References 26 publications

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“…Second, lowering the temperature from 35 to 25ЊC also did not affect either the sADP or the PP (see Crépel et al, 1994). Because the Na ϩ /Ca 2ϩ exchanger is highly temperaturesensitive (Kimura and Reeves, 1979), this latter experiment also suggests that this mechanism plays a negligible role in sADP and PP genesis. Another possible mechanism that may have contributed to the sADP and PP is deactivation of a K ϩ conductance by maintained Ca 2ϩ influx (Constanti and Bagetta, 1991;Constanti et al, 1993).…”

Section: Discussionmentioning

confidence: 77%

“…In all cases, a decrease of 10ЊC did not depress either the sADP or the PP. Because the Na ϩ /Ca 2ϩ exchanger is extremely temperature-sensitive (Kimura and Reeves, 1979;see Crépel et al, 1994), this second set of experiments also implies that the Na ϩ /Ca 2ϩ exchanger played a negligible role in genesis of the sADP and PP. Interestingly, if the bath temperature was lowered to 21-23ЊC, the PP could not be elicited (data not shown; n ϭ 3).…”

Section: Ionic Mechanisms Underlying the Sadp And Ppmentioning

confidence: 95%

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Cholinergic-Dependent Plateau Potential in Hippocampal CA1 Pyramidal Neurons

1996

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Cholinergic stimulation of the hippocampal formation results in excitation and/or seizure. We report here, using whole-cell patch-clamp techniques in the hippocampal slice (34 -35°C), a cholinergic-dependent slow afterdepolarization (sADP) and long-lasting plateau potential (PP). In the presence of 20 M carbachol, action potential firing evoked by weak intracellular current injection elicited an sADP that lasted several seconds. Increased spike firing evoked by stronger depolarizing stimuli resulted in long-duration PPs maintained close to Ϫ20 mV. Removal of either Na ϩ or Ca 2ϩ from the external media, intracellular Ca 2ϩ ([Ca 2ϩ ] i ) chelation with 10 mM bis(2-aminophenoxy)ethane-N,N,NЈ,NЈ-tetra-acetic acid, or the addition of 100 M Cd 2ϩ to the perfusate abolished both the sADP and PP. The sADP was depressed and the PP was abolished by either 10 M nimodipine or 1 M -conotoxin, whereas 1.2 M tetrodotoxin was ineffective. The involvement of a Na ϩ /Ca 2ϩ exchanger was minimal because both the sADP and PP persisted after equimolar substitution of 50 mM Li ϩ for Na ϩ in the external media or reduction of the bath temperature to 25°C. Finally, in the absence of carbachol the sADP and PP could not be evoked when K ϩ channels were suppressed, suggesting that depression of K ϩ conductances alone was not sufficient to unmask the conductance. Based on these data, we propose that a Ca 2ϩ -activated nonselective cation conductance was directly enhanced by muscarinic stimulation. The sADP, therefore, represents activation of this conductance by residual [Ca 2ϩ ] i , whereas the PP represents a novel regenerative event involving the interplay between high-voltage-activated Ca 2ϩ channels and the Ca 2ϩ -activated nonselective cation conductance. This latter mechanism may contribute significantly to ictal depolarizations observed during cholinergic-induced seizures.

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Section: Discussionmentioning

confidence: 77%

Section: Ionic Mechanisms Underlying the Sadp And Ppmentioning

confidence: 95%

Cholinergic-Dependent Plateau Potential in Hippocampal CA1 Pyramidal Neurons

1996

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“…The Na current was fitted by eqn. (3) of Kimura & Meves (1979) which is derived from and contains the four adjustable parameters I"NIa Tm, h. and Th. For Th the value 3*314 msec was found which is similar to the values 3-389 and 3 405 in Fig.…”

Section: Critical Evaluation Of the Methodsmentioning

confidence: 99%

“…In most experiments the currents were recorded on-line with a PDP 11 computer (Digital Equipment Corporation, Maynard, Mass. ) and stored on cartridge disks (see Kimura & Meves, 1979).…”

Section: Methodsmentioning

confidence: 99%

The time course of sodium inactivation in squid giant axons.

Gillespie¹,

Meves²

1980

The Journal of Physiology

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SUMMARY1. The time course of Na inactivation was studied in intact and perfused squid giant axons under voltage-clamp conditions.2. The pulse programme consisted of a conditioning pulse of varying duration, followed after an interval of 3-8 msec by a test pulse. The measurements were done in sea water with 1/3 or 1/5 of the normal Na concentration. In most experiments a 100 ssec conditioning pulse was sufficient to reduce INa peak elicited by the test pulse. In some experiments even a 50,sec conditioning pulse produced a clear reversible decrease of INa peak, We conclude that the upper limit for an initial delay in the development of inactivation is 50-100 ,usec; this applies to temperatures between 0 and 13 C and membrane potentials between -40 and 15 mV. The decrease of INa peak with increasing duration of the conditioning pulse was consistent with an exponential decay starting at 50 or 100 Itsec.3. With large Na currents in full Na sea water the time course of inactivation became sigmoid. This is attributed to a long-lasting tail of inward current which follows the conditioning pulse and produces a voltage drop across the series resistance.4. If the conditioning pulse and the test pulse were not separated by an interval,

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“…External solutions were delivered through a heat exchanger at flow rates in excess of 1Omlmin-. Internal perfusion was by a modification of the Tasaki technique, as described by Haydon & Kimura (1981 Kimura & Meves (1979) and the numerical analysis of the sodium currents were as described by Haydon & Kimura (1981). The double pulse protocol employed to investigate use dependence was as in Elliott et al (1985).…”

Section: Methodsmentioning

confidence: 99%

The effects of external and internal application of disopyramide on the ionic currents of the squid giant axon

Elliott

Hendry

1987

British J Pharmacology

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1 The actions of the class I anti-arrythmic agent, disopyramide, on the ionic currents of the voltageclamped squid axon have been investigated, by use of both extra-axonal and intra-axonal routes of application. 2 Extra-axonal application of0.1 mM disopyramide produced no significant effects on the membrane currents. External disopyramide at 1.0 mM caused small, poorly reversible inhibition of both sodium and potassium currents. This block was use-dependent and was enhanced by use of test stimuli to more positive membrane potentials. 3 Intra-axonal application of 0.1 mM disopyramide caused a 40% reduction in the first-pulse sodium current (tonic block) and an additional use-dependent block. Analysis offirst-pulse currents in terms of the Hodgkin-Huxley formalism indicated that the block resulted mainly from a reduction in the maximum available sodium conductance (gNa); there were no effects on the voltage dependence of the steady-state activation and inactivation parameters, m,, and h,. 4 The use-dependent actions of disopyramide were investigated with a double voltage-clamp pulse protocol. The significant use-dependent effects of the drug were a further reduction in ga and an increase in the time constant of inactivation (Th).5 Disopyramide appears to enter a blocking site in the sodium channel which is only readily accessible from the axoplasmic phase. Partition to the site depends on membrane voltage and on the state of the channel gates. Disopyramide binds at a significant rate to both open and inactivated forms of the sodium channel.

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The effect of temperature on the asymmetrical charge movement in squid giant axons.

Cited by 115 publications

References 26 publications

Cholinergic-Dependent Plateau Potential in Hippocampal CA1 Pyramidal Neurons

Cholinergic-Dependent Plateau Potential in Hippocampal CA1 Pyramidal Neurons

The time course of sodium inactivation in squid giant axons.

The effects of external and internal application of disopyramide on the ionic currents of the squid giant axon

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