Ouabain augments calcium‐dependent potassium conductance in visceral primary afferent neurones of the rabbit.

Higashi, Hideho; Katayama, Yoshifumi; Morita, Kenichi; North, Richard

doi:10.1113/jphysiol.1987.sp016675

Cited by 11 publications

(2 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In nodose and dorsal root ganglion cells there is evidence that calcium ionophores produce a membrane hyperpolarization and an outward current by allowing calcium ions to enter the neurone and activate a calcium-dependent potassium conductance (Higashi, Katayama, Morita & North, 1987;. In myenteric AH neurones A23187 also caused a membrane hyperpolarization associated with a decrease in input resistance.…”

Section: Discussionmentioning

confidence: 99%

Substance P inhibits activation of calcium‐dependent potassium conductances in guinea‐pig myenteric neurones.

Morita

Katayama

1992

The Journal of Physiology

Self Cite

View full text Add to dashboard Cite

SUMMARY1. Intracellular recordings were made from myenteric AH neurones of the guineapig ileum in vitro. Some experiments were done with a single-electrode voltage clamp to measure membrane currents.2. Substance P (SP) applied by superfusion (10 nM-300 nM), pressure ejection (100 nM-10 ftM, 760 mmHg, for 10-20 ms) or ionophoresis (1 mm, 100 nA, for 0-2 s) caused a membrane depolarization and an inward current, associated with a decrease in potassium conductance.3. The SP-induced depolarization was abolished within 15 min by superfusion with calcium-free/high-magnesium (10 mM) solution or solutions containing cobalt, manganese or nickel at 1-3 mm. The response persisted even after 40-60 min of superfusion with calcium-free/normal-magnesium (1-2 mM) solution. In all these solutions, synaptic potentials were abolished within 5 min.4. SP inhibited a slowly developing outward current and an outward tail current during and after a long depolarizing command pulse (2-10 s), and an outward aftercurrent following single or multiple brief depolarizing command pulses (10-50 ms). These outward currents were suppressed in calcium-free/high-magnesium solution.5. SP depressed both a calcium-dependent slow after-hyperpolarization following the action potential and an outward after-current preceded by a brief depolarizing command. Both the SP-induced depolarization and the SP-induced inward current were augmented when the peptide was pressure-ejected during the recovery phase of the slow after-hyperpolarization and during that of the slow outward after-current, but both of them were inhibited or almost abolished when SP was applied immediately after spike initiation or a brief depolarizing command.6. The SP-induced response was depressed by barium (1-2 mM). The SP response was not inhibited by tetraethylammonium at low concentrations (5-10 mm), but was depressed at high concentration (20 mM).7. Superfusion (1-10 nM) or pressure application of a calcium ionophore, A23187, inhibited or even reversed the SP depolarization and the SP-induced inward current.8. These results indicate that SP inhibits activation of a calcium-dependent potassium conductance which contributes to both the slow after-hyperpolarization MS 8113

show abstract

Section: Discussionmentioning

confidence: 99%

Substance P inhibits activation of calcium‐dependent potassium conductances in guinea‐pig myenteric neurones.

Morita

Katayama

1992

The Journal of Physiology

Self Cite

View full text Add to dashboard Cite

show abstract

“…Of relevance might be the recent report that ouabain augments a Ca2l-dependent K+ conductance in rabbit primary afferent neurones (Higashi, Katayama, Morita & North, 1987); it could be that the increased outward K+ gradient resulting from K+-free conditions exposes a population of muscle fibres in which PK has increased after pump inhibition.…”

Section: Removal Of External K+mentioning

confidence: 99%

The Effect of Sodium Pump Blockade and Denervation on the Steady‐state Sodium Permeability of Mouse Skeletal Muscle Fibres

1988

View full text Add to dashboard Cite

SUMMARYThe Na+ pump inhibitor ouabain produced a 25 mV depolarization of mouse extensor digitorum longus muscle fibres in 2 h. Approximately 40 % of this depolarization could be prevented by the inclusion of tetrodotoxin (TTX) in the incubation fluid, and the membrane potential of ouabain-depolarized fibres increased when external Na+ ion concentration was reduced. TTX and Na+ reduction were without effect on fibres incubated for 2 h in the control saline or on fibres depolarized by raising extemal K' ion concentration. Ouabain induced a fall in input resistance in fibres of reduced chloride conductance. Part of the depolarization induced in the majority of fibres by K'-free solutions was also TTX sensitive. These results suggest that the steady-state Na+ permeability of muscle fibres is increased after Na+ pump blockade. The ouabain-induced depolarization of skeletal muscle therefore cannot be taken as evidence for a significant contribution of an electrogenic Na+ pump to the resting membrane potential. TTX also reverses much of the depolarization which occurs after denervation of skeletal muscle. Denervation and ouabain both increase the steady-state Na+ permeability of the sarcolemma, possibly by an action on the same population of Na+ channels.

show abstract

Modulation of periodic cold receptor activity by ouabain

Schäfer

Braun

1990

Pflugers Arch.

View full text Add to dashboard Cite

The effect of ouabain on the periodic discharge pattern of feline cold receptors was studied in order to substantiate a possible contribution of Na/K pump activity to signal transduction. Afferent activity was recorded from the cold fibres of an isolated preparation of the tongue. The periodic pattern consisted of beating activity and of grouped discharges and was characterized by two parameters, the oscillation frequency and the number of impulses initiated per cycle. Ouabain (10(-7)-10(-6)M) induced in all receptors excitatory responses, consisting of a short vigorous increase of activity followed by inhibition. Thus the receptors never stabilized to or maintained a new static level of activity. The ouabain-induced responses occurred repeatedly in several receptors and were produced by remarkable stereotyped modifications of both the oscillation frequency and the number of impulses per cycle. The oscillation frequency attained peak values which increased monotonically with higher static temperatures and which were considerably greater than peak control values. The data indicate that an electrogenic Na/K pump contributes to the transducer process of cold receptors and that inhibition of this pump evidently gives rise to a depolarizing imbalance of the membrane potential, accelerating the oscillation frequency to a maximum value. Thus the oscillation frequency seems to be controlled by temperature and by membrane potential in cold receptors.

show abstract

Ouabain augments calcium‐dependent potassium conductance in visceral primary afferent neurones of the rabbit.

Cited by 11 publications

References 29 publications

Substance P inhibits activation of calcium‐dependent potassium conductances in guinea‐pig myenteric neurones.

Substance P inhibits activation of calcium‐dependent potassium conductances in guinea‐pig myenteric neurones.

The Effect of Sodium Pump Blockade and Denervation on the Steady‐state Sodium Permeability of Mouse Skeletal Muscle Fibres

Modulation of periodic cold receptor activity by ouabain

Contact Info

Product

Resources

About