A potassium contribution to the response of the barnacle photoreceptor.

Hanani, Menachem; Shaw, Christopher A.

doi:10.1113/jphysiol.1977.sp011943

Cited by 53 publications

(34 citation statements)

References 29 publications

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“…In this regard it is of some interest that quinine and related drugs, which block the effects of ATP in many tissues (Burnstock, 1972) also specifically uncouple increases of intracellular calcium levels from the activation of the (calcium-dependent) potassium channels (ArmandoHardy, Ellory, Ferreira, Fleminger & Lew, 1975; B.J.P. 70/3-F Hanani & Shaw, 1977). It is therefore feasible that the release or local mobilization of a purine derivative such as ATP could form the link between intracellular calcium levels and potassium channels.…”

Section: Discussionmentioning

confidence: 99%

4‐aminopyridine Blockade of Neuronal Depressant Responses to Adenosine Triphosphate

Perkins

Stone

1980

British J Pharmacology

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Adenosine, adenosine monophosphate and adenosine triphosphate (ATP) depressed the firing rate of neurones in the rat cerebral cortex when applied by microinontophoresis. 4‐Aminopyridine, also applied iontophoretically, blocked the depressant effects of the purines, without affecting responses to γ‐aminobutyric acid (GABA). This blockade was effected against purine depressions of both spontaneous and glutamate‐evoked activity, suggesting that the interaction occurred postsynaptically.

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Section: Discussionmentioning

confidence: 99%

4‐aminopyridine Blockade of Neuronal Depressant Responses to Adenosine Triphosphate

Perkins

Stone

1980

British J Pharmacology

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“…l b in Burgess et al 1979). Rather large concentrations of quinine were needed, blockade of K loss induced by A23187 being complete at 1 mm and half-maximal at Lew & Ferreira (1978) and Hanani & Shaw (1977) respectively. Similar experiments were carried out with apamin.…”

Section: Inhibitory Effects Of Quinine and Apaminmentioning

confidence: 99%

“…In the present work this effect on K movement has been shown to occur in guinea-pig hepatocytes, and the underlying changes in Ca flux initiated by A23187 and several other agents have been examined. In addition, it has been found that the movements of K triggered by a rise in Ca are abolished by quinine, as in erythrocytes (Armando-Hardy, Ellory, Ferreira, Fleminger & Lew, 1975), barnacle photoreceptors (Hanani & Shaw, 1977) and pancreatic islet cells (Atwater, Dawson, Ribalet & Rojas, 1979). We have also observed that a bee venom neurotoxin, apamin (Habermann & Reiz, 1965;Callewaert, Shipolini & Vernon, 1968;Habermann, 1972), produces a similar uncoupling in hepatocytes though not in red cells and ghosts.…”

Section: Introductionmentioning

confidence: 99%

Effects of quinine and apamin on the calcium‐dependent potassium permeability of mammalian hepatocytes and red cells.

Burgess¹,

Claret²,

Jenkinson³

1981

The Journal of Physiology

283

181

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SUMMARY1. K-sensitive electrodes placed in the extracellular fluid have been used to show that ATP and noradrenaline cause a rapid loss of up to 10 % of the K content of isolated guinea-pig hepatocytes.2. The hypothesis that this response is a consequence of a rise in the K permeability of the hepatocyte membrane triggered by an increase in cytosolic Ca is supported by the finding that the divalent cation ionophore A23187 also initiated K loss, in this instance of up to 20-25 % of the amount in the cells.3. Under similar conditions A23187 caused a transient increase, followed by a larger decrease, in the 45Ca content of guinea-pig hepatocytes equilibrated with this isotope. The decrease alone was seen with ATP and noradrenaline.4. Quinine (1 mM) and the bee venom neurotoxin apamin (10 nM) greatly reduced the effect of ATP, noradrenaline and A23187 on K content without affecting the changes in 45Ca movement.5. Apamin (10 nM) also abolished the increase in 42K efflux which follows the application of the a-adrenoceptor agonist amidephrine to rabbit liver slices; the concurrent rises in 45Ca efflux and glucose release were unaffected.6. It was concluded that quinine and apamin are able to block either the Ca-dependent K channels present in guinea-pig and rabbit liver cell membranes or the mechanism that controls them.7. Surprisingly, rat hepatocytes took up rather than lost K when treated with the concentrations of ATP, noradrenaline or A23187 that initiated K loss from guinea-pig cells. This response was greatly reduced by ouabain.8. Application of large concentrations of A23187 to rat hepatocytes caused K loss associated with cell death.9. The influence of apamin (10-1000 nM) and quinine (200-1000 UM) on the Ca-dependent K permeability of red blood cells and ghosts was also studied. Apamin was without effect even when applied to both sides of the ghost membrane, whereas quinine caused inhibition, as reported by others.10. The results suggest that Ca-dependent K channels or carriers are present in

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“…There is abundant evidence, however, particularly at high light intensities and during prolonged illumination, that non-light dependent changes in membrane permeability occur which modify the shape of the receptor potential. These secondary effects result mostly from the activation of voltage-dependent permeabilities in the membrane (Naka & Eguchi, 1962;Baumann, 1968; Baylor, Hodgkin & Lamb, 1974; Werblin, 1975;Hanani & Shaw, 1977;Pepose & Lisman, 1978;Fain, Quandt & Gerschenfeld, 1977). Because these secondary changes in membrane potential form part of the signal conveyed by the receptor about light it is important to separate clearly light dependent from non-light dependent changes in permeability.…”

Section: Introductionmentioning

confidence: 99%

Contribution of calcium and potassium permeability changes to the off response of scallop hyperpolarizing photoreceptors.

Cornwall¹,

Gorman²

1979

The Journal of Physiology

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SUMMARY1. The membrane response of the distal photoreceptors in the retina of the scallop Pectin irradians to the termination of a bright white light (off response) is shown to be composed of the decay of the hyperpolarizing receptor potential and an action potential with slow kinetics.2. The action potential can be produced in darkness in the absence of external Na+ ions by membrane depolarization.3. The action potential is maintained by replacement of external Ca2+ with Sr2+ or Ba2+, but not by Mg2+. In normal external Ca2+ (9 mM), the action potential is abolished by the addition of the Ca2+ inhibitors, La3+, Co2+, and Mn2+ or the organic Ca2+ antagonist D-600.4. Elevated external Ca2+ concentrations increase the rate of rise and peak amplitude of the action potential as well as the rate of repolarization and after hyperpolarization, but decrease the duration.5. The rate of rise and peak amplitude of the action potential are increased by the K+ antagonists tetraethylammonium (TEA) 4-amino-pyridine (4-AP), Ba2+ and procaine. The antagonists have different effects on subsequent phases of the response, however. External TEA and Ba2+ increase the duration, but decrease the rate of repolarization and abolish the after hyperpolarization, whereas external 4-AP and procaine increase the rate of repolarization, decrease the duration and increase the after hyperpolarization.6. The ratio of the Ca2+ to K+ permeability (PC/0PK) estimated from the constant field equation at the peak of the action potential in different external Ca2+ concentrations is close to 1. 7. The maximum rate of rise and the peak amplitude of the action potential are increased by membrane hyperpolarization and decreased by membrane depolarization. They are decreased by background light intensity relative to their value in the dark.8. In normal ASW the action potential can be identified during the off response as a small overshoot of membrane potential relative to its value in the dark.9. The rate of repolarization of the off response in normal ASW is reduced by agents or conditions which inhibit or reduce Ca2+ permeability changes, e.g. external Co2+ and La2+ or zero external Ca2+.

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A potassium contribution to the response of the barnacle photoreceptor.

Cited by 53 publications

References 29 publications

4‐aminopyridine Blockade of Neuronal Depressant Responses to Adenosine Triphosphate

4‐aminopyridine Blockade of Neuronal Depressant Responses to Adenosine Triphosphate

Effects of quinine and apamin on the calcium‐dependent potassium permeability of mammalian hepatocytes and red cells.

Contribution of calcium and potassium permeability changes to the off response of scallop hyperpolarizing photoreceptors.

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