Accelerating effects of pentobarbitone on the inactivation process of the calcium current in <i>Helix</i> neurones

Nishi, Katsuhide; Oyama, Yasuo

doi:10.1111/j.1476-5381.1983.tb10001.x

Cited by 25 publications

(19 citation statements)

References 18 publications

(18 reference statements)

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“…For methohexitone the situation is more complex, since the inhibition of the peak current caused by application of methohexitone developed over many seconds and successive stimuli intensified the inhibition (Fig. 2C) (Nishi & Oyama, 1983 b). Later they revised this interpretation and proposed that the increased current decay reflected an enhanced rate of voltage-dependent inactivation (Nishi & Oyama, 1983 a).…”

Section: Discussionmentioning

confidence: 99%

“…2C) (Nishi & Oyama, 1983 b). Later they revised this interpretation and proposed that the increased current decay reflected an enhanced rate of voltage-dependent inactivation (Nishi & Oyama, 1983 a). Although Werz & Macdonald (1985) also found that pentobarbitone and phenobarbitone enhanced calcium current decay in mouse dorsal root ganglion cells maintained in culture, they felt that the evidence was not sufficient to distinguish between these mechanisms; a conclusion we endorse.…”

Section: Discussionmentioning

confidence: 99%

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Calcium channel currents in bovine adrenal chromaffin cells and their modulation by anaesthetic agents.

Charlesworth

Pocock

Richards

1994

The Journal of Physiology

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1. The calcium channel currents of bovine adrenal chromaffin cells were characterized using a variety of voltage pulse protocols and selective channel blockers before examination of their modulation by anaesthetic agents. 2. All the anaesthetics studied (halothane, methoxyflurane, etomidate and methohexitone) inhibited the calcium channel currents in a concentration‐dependent manner and increased the rate of current decay. 3. The anaesthetics did not shift the current‐voltage relation nor did they change the voltage for half‐maximal channel activation derived from analysis of the voltage dependence of the tail currents. None of the anaesthetics appeared to alter the time constant of tail current decay. 4. To complement earlier studies of the inhibitory actions of anaesthetics on K(+)‐evoked catecholamine secretion and the associated Ca2+ uptake, the IC50 values for etomidate and methohexitone were determined using a biochemical assay. The IC50 values for anaesthetic inhibition of calcium channel currents corresponded closely with those for inhibition of K(+)‐evoked calcium uptake and catecholamine secretion. 5. The inhibitory effect of the volatile anaesthetics and etomidate is best explained by dual action: a reduction in the probability of channel opening coupled with an increase in the rate of channel inactivation. Methohexitone appeared to inhibit the currents by a use‐dependent slow block.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Calcium channel currents in bovine adrenal chromaffin cells and their modulation by anaesthetic agents.

Charlesworth

Pocock

Richards

1994

The Journal of Physiology

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“…A local anaesthetic, such as lignocaine, also accelerated slightly the decay phase of ICa during long depolarizing pulses (Oyama & Nishi, unpublished observations). Thus, other mechanisms to explain the accelerating action of pentobarbitone on the decay phase of ICa as discussed in the previous paper (see Nishi & Oyama, 1983) were unlikely. Therefore, we conclude that barbiturates accelerate nonspecifically the decay phase of ICa by increasing the rate of the voltage-dependent inactivation which would be induced by conformational changes in the lipid milieu surrounding the calcium channel.…”

Section: Effects Ofbarbiturates On the Calcium Currentmentioning

confidence: 99%

“…We have previously shown that pentobarbitone accelerates the decay phase of the calcium current (ICa) in Helix neurones (Nishi & Oyama, 1983). The accelerating action of pentobarbitone on the decay phase of ICa was reminiscent of the accelerated decay phase of the sodium current (INa) seen with the internal presence of pancuronium molecules (Yeh & Narahashi, 1977).…”

Section: Introductionmentioning

confidence: 99%

“…in molluscan neurones is not only voltage-dependent but also current-dependent (Brehm & Eckert, 1978;Tillotson, 1979;Brehm, Eckert & Tillotson, 1980;Brown, Morimoto, Tsuda & Wilson, 1981;Plant & Standen, 1981). Therefore, explanations for the mode of the accelerating action of pentobarbitone on the decay phase of "Ca must be more complicated than those for pancuronium on the INa (Nishi & Oyama, 1983). …”

Section: Introductionmentioning

confidence: 99%

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Barbiturates increase the rate of voltage‐dependent inactivation of the calcium current in snail neurones

Nishi

Oyama

1983

British J Pharmacology

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Effects of barbiturates (thiopentone, pentobarbitone, phenobarbitone and barbitone) on the calcium current (ICa) in identified Helix neurones were studied, using a conventional suction pipette technique. Barbiturates depressed the maximal peak amplitudes (MPA) of ICa in a dose‐dependent manner without shifting the current‐voltage relationships along the voltage axis. Barbiturates accelerated the decay phase of ICa at high concentrations (1 × 10−4 to 3 × 10−3 m), at which concentrations double‐pulse experiments showed the increased rate of a voltage‐dependent inactivation of ICa. It is concluded that the acceleration of the decay phase of ICa by barbiturates may be due to the increased rate of the voltage‐dependent inactivation of ICa.

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Postsynaptic Actions of Pentobarbital in Cultured Mouse Spinal Neurons and Rat Hippocampal Neurons

Owen¹,

Barker²,

Segal³

et al. 1986

Molecular and Cellular Mechanisms of Anesthetics

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Accelerating effects of pentobarbitone on the inactivation process of the calcium current in Helix neurones

Cited by 25 publications

References 18 publications

Calcium channel currents in bovine adrenal chromaffin cells and their modulation by anaesthetic agents.

Calcium channel currents in bovine adrenal chromaffin cells and their modulation by anaesthetic agents.

Barbiturates increase the rate of voltage‐dependent inactivation of the calcium current in snail neurones

Postsynaptic Actions of Pentobarbital in Cultured Mouse Spinal Neurons and Rat Hippocampal Neurons

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