Contribution of chloride shifts to the fade of gamma‐aminobutyric acid‐gated currents in frog dorsal root ganglion cells.

Akaike, Norio; Inomata, Norio; Tokutomi, Naofumi

doi:10.1113/jphysiol.1987.sp016735

Cited by 77 publications

(44 citation statements)

References 27 publications

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“…However, at a AVH greater than 20 mV, a continuous application of GABA induced a time-dependent negative or positive shift of the reversal potential (EGAB,) depending upon the inward or outward currents. The results indicate that the decay of the GABA-induced current during GABA application at greater AVVH were the sum of 'true' receptor desensitization and Cl -shifts (Akaike et al, 1987a). We also found in the frog sensory neurones that the GABA-induced Ic, was reduced in the presence of external Na+ and that the inhibition was mediated by the uptake of GABA subserved by a Na-GABA cotransport mechanism (Akaike et al, 1987b).…”

Section: Methodssupporting

confidence: 50%

Effects of diuretics on GABA‐gated chloride current in frog isolated sensory neurones

Inomata

Ishihara

Akaike

1988

British J Pharmacology

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Effects of three diuretics (furosemide, amiloride and α‐human atrial natriuretic polypeptide (α‐hANP)) on GABA‐activated chloride current (ICl) were investigated in frog isolated sensory neurones, following suppression of Na+, K+ and Ca2+ currents, by use of a ‘concentration‐clamp’ technique. Furosemide inhibited the GABA‐activated ICl in a non‐competitive manner and facilitated the inactivation phase, while amiloride inhibited the GABA response in a competitive manner, both inhibitions being concentration‐dependent. α‐hANP had no effects on the GABA‐induced ICl. The reversal potential of GABA‐activated ICl (EGABA) was not shifted in the presence of amiloride or furosemide. The results suggest that amiloride may act at the GABA binding site while furosemide may act on the GABA‐gated chloride channel.

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Section: Methodssupporting

confidence: 50%

Effects of diuretics on GABA‐gated chloride current in frog isolated sensory neurones

Inomata

Ishihara

Akaike

1988

British J Pharmacology

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“…Fig. 1 of Nakahiro et al 1989), due to receptor desensitization and/or alterations in intracellular Cl- (Numann & Wong, 1984;Akaike, Inomata & Tokutomi, 1987). In our initial experiments, when GABA was applied at high pipette concentrations, or over very long application times, the GABA response 'faded' rapidly, and anaesthetic-induced enhancement of IGABA was often absent.…”

Section: Discussionmentioning

confidence: 99%

Enhancement of gamma‐aminobutyric acid‐activated Cl‐ currents in cultured rat hippocampal neurones by three volatile anaesthetics.

Jones

Brooks

Harrison

1992

The Journal of Physiology

188

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SUMMARY1. The effects of the volatile anaesthetics enflurane, halothane and isoflurane on yaminobutyric acid (GABA)A receptor-mediated chloride currents were studied in cultured rat hippocampal neurones. Transient current responses were obtained by brief pressure application of GABA to the cell body of neurones under voltage clamp.2. All three anaesthetics increased the peak amplitude and duration of current responses to brief applications of GABA. These effects were fully reversible, and did not involve alterations in the reversal potential for GABA responses.3. The experimental concentrations of anaesthetics were measured directly using gas chromatography. The enhancement of GABA currents increased with increasing anaesthetic concentration. Clinically effective concentrations of anaesthetics (between 1 and 1-5 times MAC (minimum alveolar concentration) produced significant enhancement of GABA currents.4. These results demonstrate that the changes in the time course of synaptic inhibition reported in the presence of the volatile anaesthetics are likely to result from modification of the function of postsynaptic GABAA receptor-channel complexes. These findings also support the hypothesis that GABAA receptor complexes serve as common molecular target sites for a variety of structurally diverse anaesthetic molecules.

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“…The sodium current (INa) in the isolated single ventricular cells was measured by using a single suction pipette which enabled intra cellular perfusion and a whole-cell clamp (11,16). Experiments were carried out with viable rod-shaped myocytes using the concentration-clamp technique (17).…”

Section: Electrical Recordingmentioning

confidence: 99%

Modes of the Na Channel Blocking Action of Pilsicainide, a New Antiarrhythmic Agent, in Cardiac Cells.

Hattori

Inomata

1992

Jpn.J.Pharmacol

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Using a whole cell clamp technique, the blockade of sodium currents (INa) by pilsicainide, a new antiarrhythmic agent, applied either intracellularly or extra cellularly, was studied in single myocytes isolated from guinea pig right ventricle. Pilsicainide applied extracellularly inhibited the peak amplitude of INa in concentration (from 105 M to 104 M) and rate (from 0.5 Hz to 3.0 Hz) dependent manners. The onset rate of the blockade in INa was almost constant, independent of frequency of stimulus, but higher at high concentration of pilsicainide. The time con stant in the recovery phase from INa inactivation remained almost constant (65 to 75 msec) in the range of concentrations used. Similar results were obtained by intracellu lar application of 10-3 M pilsicainide. Pilsicainide applied intracellularly inhibited INa in a rate-dependent manner. The blocking potency of internally applied pilsicainide almost corresponded to that of external 10-5 M pilsicainide. The onset rate of INa in activation (from 0.098/pulse to 0.130/pulse) and the recovery time constant (77 msec) was similar to those of external 10-5 M pilsicainide. These results suggest that pilsi cainide, irrespective of intra or extracellular application, shares a common binding site to block INa in cardiac myocytes.

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Contribution of chloride shifts to the fade of gamma‐aminobutyric acid‐gated currents in frog dorsal root ganglion cells.

Cited by 77 publications

References 27 publications

Effects of diuretics on GABA‐gated chloride current in frog isolated sensory neurones

Effects of diuretics on GABA‐gated chloride current in frog isolated sensory neurones

Enhancement of gamma‐aminobutyric acid‐activated Cl‐ currents in cultured rat hippocampal neurones by three volatile anaesthetics.

Modes of the Na Channel Blocking Action of Pilsicainide, a New Antiarrhythmic Agent, in Cardiac Cells.

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