Movements of labelled sodium ions in isolated rat superior cervical ganglia

Brown, David A.; Scholfield, C.N.

doi:10.1113/jphysiol.1974.sp010710

Cited by 31 publications

(27 citation statements)

References 38 publications

(80 reference statements)

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“…This was consistent with the observation (Wespi, 1969) that lithium is a poor substrate for the sodium ion pump in mammalian nonmyelinated nerve even though it can permeate membrane sodium ion channels (see Armett & Ritchie, 1963a, b) and thus carry depolarizing current in these tissues. Finally, post-5-HT hyperpolarization was selectively inhibited in potassium-free Krebs-Henseleit medium, consistent with the requirement for extracellular potassium ions for the activation of the sodium ion pump (see Brown & Scholfield, 1974). A similar inhibitory effect of potassium-free media has been described for post-carbachol and post-DMPP hyperpolarization of the rat and rabbit SCG, respectively (Brown et al, 1972;Lees & Wallis, 1974).…”

Section: Hyperpolarization Ofthe Superior Cervical Ganglionmentioning

confidence: 51%

“…An alternative explanation for the inhibitory effect of ouabain on 5-HT-induced hyperpolarization of the rat SCG is that it was an indirect result of the inhibition of Na+K+-ATPase -possibly secondary to a fall in membrane potential. Further, because rat Na+K+-ATPase seems rather insensitive to ouabain (see Aldridge, 1962;Akera et al, 1969;Brown et al, 1972;Brown & Scholfield, 1974) a very high concentration ofthe drug (1 x 1O-3M) was used in the present study. Therefore the effects of ouabain described here may have been due to some action other than inhibition of this enzyme.…”

Section: Hyperpolarization Ofthe Superior Cervical Ganglionmentioning

confidence: 99%

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Origin of 5‐hydroxytryptamine‐induced hyperpolarization of the rat superior cervical ganglion and vagus nerve

Ireland

1987

British J Pharmacology

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1 5-Hydroxytryptamine (5-HT)-induced membrane potential changes were recorded extracellularly from rat superior cervical ganglia (SCG) and cervical vagus nerves in vitro. 2 On the SCG, low concentrations of 5-HT (I x 10-8-3 x 10-7M) induced concentration-related hyperpolarization responses. Higher concentrations of 5-HT (I x 10-6_1 X 10-4M) induced complex responses which typically consisted of an initial hyperpolarization, followed by a depolarization and subsequent after-hyperpolarization. The depolarization, but not the initial hyperpolarization, was blocked by metoclopramide (3 x 10-5M), quipazine (1 x 10-6M) or MDL 72222 (1 x 10-5M). 3 5-HT-induced hyperpolarization of the SCG was potentiated when the amount ofcalcium chloride added to the superfusion medium was reduced from 2.5 to 0.15 mmol 1 -'. Hyperpolarization responses recorded from SCG preparations superfused with this low-calcium medium were unaffected by the substitution oflithium chloride for sodium chloride and were potentiated by the omission ofpotassium ions. Ouabain (1 x 10-3M) abolished both the hyperpolarization and the depolarization induced by 5-HT. 4 On the vagus nerve, 5-HT (1 x 10 -3 x 1I0-M) did not induce initial hyperpolarization in either normal or low-calcium Krebs-Henseleit medium. However, in the latter solution only, depolarization responses induced by 5-HT at concentrations of 1 x 10-6M or greater were followed by hyperpolarization. Both the depolarization and the post-5-HT hyperpolarization were blocked by metoclopramide (3 x 10-5M) but were unaffected by spiperone (1 x 10-7M). 5 On the vagus nerve, post-5-HT hyperpolarization responses were selectively and reversibly inhibited by ouabain, and by superfusion with Krebs-Henseleit medium that was either potassium-free or contained lithium chloride in place of sodium chloride. 7 These results demonstrate the generation in the rat SCG of a 5-HT-induced hyperpolarization response that is not mediated through 5-HT3 receptors and is unlikely to be a consequence of depolarization. In contrast, on the rat vagus nerve, the post-5-HT hyperpolarization observed in the present study had the characteristics expected of depolarization-dependent activation of a sodium ion pump.

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Section: Hyperpolarization Ofthe Superior Cervical Ganglionmentioning

confidence: 51%

Section: Hyperpolarization Ofthe Superior Cervical Ganglionmentioning

confidence: 99%

Origin of 5‐hydroxytryptamine‐induced hyperpolarization of the rat superior cervical ganglion and vagus nerve

Ireland

1987

British J Pharmacology

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“…When the carbachol is washed out, a hyperpolarization follows due to the activity of an electrogenic Na-K exchange pump (Brown, Brownstein & Scholfield, 1972). The movements of Na accompanying these changes have been examined in some detail (Brown & Scholfield, 1974b), but studies of K movements were limited to the destructive analysis of ganglia for total ion contents (Brown & Scholfield, 1974a). The aim of the present study was to monitor the 42K or 86Rb content of single ganglia by a continuous flow method of the kind described by Brinley (1967).…”

Section: Introductionmentioning

confidence: 99%

“…3A). On washing out the carbachol and superfusing with 2-5 mm hexamethonium (to arrest the residual carbachol action; see Brown & Scholfield, 1974b and Fig. 4), the lost 86Rb was regained with a half-time of about 10 min (Fig.…”

Section: Introductionmentioning

confidence: 99%

Movements of radioactive potassium in isolated rat ganglia

Scholfield

1977

The Journal of Physiology

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SUMMARY1. Isolated rat superior cervical ganglia were continuously superfused with 42K (or 86Rb) solution and the amount of radioactivity taken up was monitored using scintillation counting.2. Entry of 42K into the ganglia could be resolved into two components, one amounting to 83 % of the total 42K uptake, with a rate constant of 0.015 min-, and the other of 17 % of the total, with a rate constant of 0-15 min-.3. With 6 mM-K in the bathing solution, the equilibrium uptake of 42K after 4 hr corresponded to an intracellular concentration of 147 mM-K.Changes in the K concentration of the bathing solution (0.5-20 mM) had little effect on this value.4. Carbachol or nicotine caused a rapid net loss of 42K. 42K was recaptured on washing out the depolarizing agents, with a rate constant of about 0*3 min-'. This recapture rate was slowed by ouabain, dinitrophenol, cyanide, mersalyl and by reducing the K concentration in the bathing solution.5. Efflux of 42K from preloaded ganglia occurred with a rate constant of 0-017 min-'. This rate was increased about sixfold by 180 /SM carbachol in 6 mM-K but not in 150 mM-K suggesting that the increase in efflux was mainly a consequence of the depolarization caused by carbachol.6. 86Rb fluxes and the effects of carbachol thereon were similar.

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“…This is as predicted by the Goldman Constant-Field Equation (Goldman, 1943) and is different from the [K+] dependence of the Na/K pump which decreases as extracellular [K+] increases (Henn, Haljamae & Hamberger, 1972;Brown & Scholfield, 1974).…”

Section: Hypoxia On Hippocampal-evoked Potentials Effect Of Differentmentioning

confidence: 99%

The effect of hypoxia on evoked potentials in the in vitro hippocampus.

Lipton¹,

Whittingham²

1979

The Journal of Physiology

117

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SUMMARY1. We have studied the effect of hypoxia on transmission of electrical activity between the perforant path and the dentate granule cells in the in vitro guinea-pig hippocampus.2. Hypoxia abolishes the evoked field potential within about 3 min, a time similar to that occurring in vivo (Andersen, 1960).3. The evoked potential is very rapidly abolished by extracellular K+ concentrations greater than 13 4 mM; it is abolished by ouabain concentrations greater than 10-5 M. The rate at which it is abolished increases with increasing ouabain concentrations; concentrations of about 8 x 10-5 M abolish the evoked potential at the same rate as does hypoxia.4. The time required to abolish the evoked potential during hypoxia decreases markedly as the extracellular K+ concentration is elevated from 4.4 to 13-4 mM. The time to abolish the potential during hypoxia is also decreased by partial replacement of the Cl-in the bathing medium by less permeant anions and by the presence of a low (10-7 M) concentration of ouabain. All these are conditions which are expected to depolarize neuronal cell membranes. None of these alterations in the perfusing medium affect the concentrations of ATP or creatine phosphate in the hippocampal slice. Increasing extracellular Mg2+/Ca2+ to levels which reduce the evoked response by about 50 % has no effect upon the time required to abolish the evoked potential during hypoxia at any concentration of extracellular [K+].5. These results provide evidence that the basis for the hypoxic block of the evoked potential is a depolarization of neuronal processes. They are consistent with the hypothesis that this depolarization is a result of inhibition of the Na+/K+ pump.

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Movements of labelled sodium ions in isolated rat superior cervical ganglia

Cited by 31 publications

References 38 publications

Origin of 5‐hydroxytryptamine‐induced hyperpolarization of the rat superior cervical ganglion and vagus nerve

Origin of 5‐hydroxytryptamine‐induced hyperpolarization of the rat superior cervical ganglion and vagus nerve

Movements of radioactive potassium in isolated rat ganglia

The effect of hypoxia on evoked potentials in the in vitro hippocampus.

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